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Abstrak :
Latar Belakang. Cedera Reperfusi Iskemia merupakan eksaserbasi paradoks mengakibatkan disfungsi dan kematian sel setelah aliran darah direstorasi ke jaringan yang sebelumnya iskemia. Pada iskemia tungkai akut, reperfusi menimbulkan reaksi kompleks melibatkan inflamasi lokal maupun sistemik dengan dampak lokal sindroma kompartemen dan dampak sistemik berupa disfungsi hingga kegagalan multi organ. Platelets activating factors (PAF) sebagai mediator inflamasi pospholipid mempunyai efek fisiologis yang poten dan beragam, sehingga meningkatkan respon inflamasi pada cedera reperfusi iskemik. Berbagai upaya untuk mencegah dan memperingan cedera reperfusi iskemik, antara lain penggunaan prosedur ischemic preconditioning, antioksidan dan terapi anti-sitokin telah diteliti namun hasil dan manfaat klinisnya belum memuaskan. PTX, phosphodiesterase nonspesifik derivat xanthine, memperlihatkan efek penekanan inflamasi dan menghambat interaksi lekositendotel yang menjanjikan dalam mencegah cedera reperfusi. Namun hasil penelitian mengenai peran pentoxifylinne dalam menekan reaksi inflamasi melalui penekanan PAF pada iskemia tungkai akut tidak konsisten. Sehingga penelitian ini bertujuan untuk menilai peran PTX dalam mengurangi cedera reperfusi melalui penekanan mediator inflamasi PAF pada hewan coba kelinci dengan Reperfusi Iskemia tungkai akut. Metodologi. Dilakukan tindakan iskemik tungkai kiri selama 3 jam yang diikuti 2 jam periode reperfusi pada 10 ekor kelinci New Zealand White jantan yang dibagi menjadi 2 kelompok (kelompok pentoksifin dan kelompok kontrol) secara acak. Pada kelompok perlakuan diberikan PTX 30 menit sebelum reperfusi dengan dosis initial bolus 40 mg/kgBB diikuti dengan dosis rumatan 1 mg/kg BB/jam hingga 3 jam periode reperfusi. Pada kelompok kontrol diberikan cairan garam fisiologis dengan kecepatan dan volume yang sebanding. Tindakan Iskemik dilakukan dengan oklusi arteri iliaka komunis sinistra mengunakan klem selama 3 jam kemudian dilanjutkan dengan restorasi aliran darah. Pengambialn sampel untuk pemeriksaan kadar PAF dilakukan pada 2,5 jam iskemik dan pada 2 jam reperfusi. Hasil. Pada periode Iskemik dua jam tiga puluh menit tidak mengakibatkan perbedaan bermakna (p=0,754), kadar rerata PAF pada kelompok PTX 13,09 ± 0,41 pg/mL dan kelompok kontrol I3,38 ± 0,28 pg/mL. Pada jam ke dua tindakan reperfusi ditemukan perbedaan bermakna (p=0,009) kadar rerata PAF dari kelompok PTX menurun menjadi 11,36±0,78 pg/mL dan kelompok kontrol meningkat menjadi 25,5±0,78 pg/dL. Kesimpulan. PTX menurunkan kadar PAF plasma kelinci dengan cedera reperfusi iskemikia tungkai akut.

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Background. Ischemic reperfusion injury is a paradoxical exacerbation of cell dysfunction and death following the restoration of blood flow to previously ischemic tissue. Restoration of blood flow is essential to salvage ischemic tissue, however reperfusion itself paradoxically causes further damage to the ischemic tissue, threatening function and viability both organ local and distal through the inflammation response. In Acute limb ischemia, there are essentially two components: a local component that can result in increasing the regional damage from ischemia inflammatory responses which may result in local syndrome, compartment syndrome, and systemic syndrome, multi organ dysfunction and failure. Several method and attempt had been studied and performed to prevent and attenuate reperfusion injury such as, ischemic preconditioning, antioxidant, and anti-cytokine therapy, but their clinical benefit were not satisfactory. Pentoxifylline has emerged as an agent that may attenuate inflammation response through several mechanisms. However, studies on PTX and its function to prevent and attenuate inflammation response through attenuating PAF in acute limb ischemic were not consistent. In this study the role of PTX and its function to prevent and attenuate inflammation response through attenuating PAF in acute limb ischemic was investigated. Methods. Acute limb ischemia in the left lower limbs of 10 New Zealand White male rabbit were performed for 3 hour followed by 2 hours period of ischemia. The rabbits were randomly separated into 2 groups of five (group pentoxifylinne and group control). The Pentoxifylline group was given PTX 40 mg/kg bolus half an hour prior to reperfusion followed by maintenance dose 1 mg/kg/hour until 2 hour post reperfusion, while the control group was given normal saline solution with comparable volume and rate administration. Acute limb Ischemic procedure was performed by direct occlusion of the left femoral artery using non traumatic clamp and followed by releasing the clamp after 3 hours of occlusion. Level of PAF were measured after 2.5 hour of ischemic period and after 2 hours of reperfusion period. Results. After 2.5 hours of ischemic period, the mean PAF levels did not show any significant difference (p=0.754). The mean PAF level of pentoxifylline group 13.09f0.41 pg/mL, while the mean PAF level of control group 13.38±0.28 pg/mL, After 2 hours period of reperfusion, there were significant differences of mean PAF level between the two groups (p=0.009). The mean PAF level in the control group increase by 12.1 110.79 to became 25.5±0.78 pg/dL, while the mean PAF level of the PTX group decrease by 1.73f1.1 pg/mL and became 11.36±0.78 pg/m L. Conclusion. PTX decreased the PAF level in rabbits with acute limb ischemic reperfusion injury.

Abstrak :
Latar Belakang. Komplikasi tindakan revaskularisasi pasca suatu periode iskemik mulai menjadi perhatian kalangan medis sejak awal abad ke-20. iskemik tungkai akut merupakan masalah kegawatan kardiovaskular dan tindakan reperfusi terhadap jaringan yang iskemik ternyata sexing memperburuk cedera jaringan yang ada, bahkan sampai dilakukan amputasi. Pada ceders reperfusi iskemik (R-1) terjadi perubahan sifat hemoreologi darah (hematokrit, viskositas, dan deformitas set darah merah). Pentoksifilin (PTXF) mempunyai kemampuan memperbaiki cedera reperfusi dengan meningkatkan aliran darah perifer, memperbaiki deformitas sel darah merah, menurunkan viskositas darah, dan menekan agregasi platelet. Tujuan Penelitian. Untuk mengetahui pengaruh pemberian PTXF terhadap faktor hemoreologi darah pada cedera R-I tungkai akut. Metode. Penelitian dilakukan pada kelinci jantan ras New Zealand White Rabbit (NZW) yang berasal dari 1 galur sebanyak 10 ekor usia 5 bulan dengan berat badan rata-rata 2,5-3 kg. Kemudian hewan coba dibagi dalam 2 kelompok, yakni 5 ekor kelinci kelompok perlakuan diberi PTXF dengan dosis 40 mglkgBB yang diikuti dosis rumatan 1 mglkgBBljam dan 5 ekor kelinci sebagai kontrol diberi cairan NaCl 0,9% dengan kecepatan yang sama seperti kelompok perlakuan. Dilakukan oklusi arteri iliaka komunis sinistra dan setelah 2,5 jam iskemik diambil darah untuk pemeriksaan hematokrit dan viskositas, setelah itu segera diberikan PTXF. Pada jam ke-3 dilakukan reperfusi (membuka oklusi) dan 2 jam setelah reperfusi diambil darah untuk pemeriksaan hematokrit dan viskositas. Data hasil pemeriksaan dianalisis dengan statistik program SPSS 13 dengan menggunakan uji parametrik General Linear Model (GLM) untuk pengukuran berulang. Hasil. Nilai rerata hematokrit kelompok PTXF fase iskemik 37,06+3,88% dan fase reperfusi 34,20+1,90% dengan delta penurunan 2,86%. Nilai rerata hematokrit kelompok nonPTXF fase iskemik 35,88+5,31% dan fase reperfusi 32,90+4,61% dengan delta penurunan 2,98%. Antara pengukuran pertama dan kedua, baik kelompok PTXF dan nonPTXF tidak terdapat perbedaan bermakna (per, i 9 dan p=0,37). Analisis statistik nilai rerata hematokrit antara kelompok PTXF dan nonPTXF tidak terdapat perbedaan bermakna (p=0,74). Nilai rerata viskositas kelompok PTXF fase iskemik 5,25+0,77 ep dan fase referfusi 4,69+0,70 cp dengan delta penurunan 0,558 cp. Nilai rerata viskositas kelompok nonPTXF fase iskemik 4,54+0,48 cp dan fase reperfusi 4,48+1,31 cp dengan delta penurunan 0,066 cp. Antara pengukuran pertama dan kedua, baik, kelompok PTXF dan nonPTXF tidak terdapat perbedaan bermakna secara statistik (p~,26 dan p=0,92). Analisis statistik pada nilai rerata viskositas antara kelompok PTXF dan nonPTXF tidak terdapat perbedaan bermakna (p=0,53). Kesimpulan. Pemberian PTXF pada kelompok perlakuan memperlihatkan hasil tidak bermakna dalam menurunkan nilai hematokrit dan viskositas darah dibanding kelompok kontrol pads keadaan ceders R-I tungkai akut.

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Background: Complications of revascularization after an ischemic period has attract attention from clinicians since the beginning of 20th century. Acute limb ischemia is an emergency cardiovascular problem and revascularization procedures of ischemic tissue has been documented to worsen tissue damage to the extend of a need for limb amputation. In ischemic reperfusion injury, changes in blood hemorheology occurs (hematocrit, viscosity and eryhtrocyte deformities). Pentoxifylline (PTXF) has the ability to repair reperfusion injury by increasing peripheral blood flow, repairing eryhtrocyte deformities, decreasing blood viscosity dan suppressing platelet agregation. Objectives: To investigate the effect of pentoxifylline administration toward hemorheology changes in acute limb ischemic reperfusion injury. Methods: We studied 10 pure strain New Zealand White Rabbit (NZW) age 5 months with mean weight of 2.5-3 kg. The subjects were divided in two groups; 5 of the experimental rabbit were given PTXF 40 mg/kg body weight followed by a maintenance dose of 1 mg/kg body weight/hour, while subjects in the control group received a similar administration of NaCl 0.9%. We performed occlusion of the left common iliac artery and after an ischemic period of 2.5 hours blood samples were taken for hematocrit and viscosity measurement. PTXF were given soon afterward. On the third hour the artery occlusion were opened and after another two hours blood samples were again taken for hematocrit and viscosity measurement. Data analysis were performed by SPSS 13, using parametric test with general linear model (GLM) for repeated measurements. Results: The mean hematocrit value for the PTXF group in the ischemic period were 37.0613.88%, and in the reperfusion period were 34.2011.90%, with a decrease of 2.86%. The mean hematocrit value for the control group in the ischemic and reperfusion period were 35.8815.31% and 32.90±4.61% , respectively, with a decrease of 2.98%. There were no significant difference between the first and second hematocrit measurements both in the experimental and control group (p-0.19 and p=0.37). Statistical analysis of mean hematocrit value between the two groups also showed no significant difference (p=0.74). The mean viscosity value for the PTXF group in the ischemic period were 5.2510.77 cp and in the reperfusion period were 4.6910.70 cp with a difference of 0.558 cp. The mean viscosity value for the control group in the ischemic and reperfusion period were 4.54±0.8 cp and 4.4811.31 cp, respectively, with a decrease of 0.066 cp. There were no statistically significant difference between the first and second viscosity measurements both in the experimental and control group (p=0.26 and p=0.92). Statistical analysis of mean viscosity value between the two groups also showed no significant difference (p=0.53). Conclusion: PTXF administration in the experimentally induced acute limb ischemic reperfusion injury in rabbits have no benefits to decrease hematocrit and viscosity values compared to control group.

Abstrak :
Latar belakang: Inflamasi memegang peranan penting dalam IMA-EST, terutama kejadia cedera reperfusi. Kolkisin merupakan sediaan obat anti inflamasi, yang dapat menekan inflamasi saat terjadi cedera reperfusi. Kami menilai keefektivan dari pemberian kolkisin pada pasien IMA-EST yang menjalani IKPP dalam menekan cedera reperfusi. Metode: Penelitian ini merupakan uji klinis, tersamar ganda, dengan plasebo, yang dilakukan multisenter di dua rumah sakit di Jakarta dengan fasilitas IKPP dari Desember 2022 hingga April 2023. Pasien IMA-EST yan menjalani IKPP diberikan dosis muat kolkisin 2 mg, kemudian dosis pemeliharaan 2x0,5 mg selama 2 hari, dan amilum pada kelompok plasebo. Pasien diamati kejadian cedera reperfusi berupa TIMI flow, kejadian aritmai, syok dan aritmia akibat reperfusi. Hasil: Sebanyak 77 subyek IMA-EST dengan rerata usia 55.2 ± 9.9 tahun menjalani IKPP. 37 subyek mendapat kolkisin, 40 subyek mendapat placebo. Kebanyakan subjek ialah laki-laki (77.5%), menderita 3 vessel disease (44,1%), oklusi di LAD ( 53,2%). Pemberian kolkisin tidak berhasil menurunkan kejadia cedera iskemia reperfusi (51.5% vs. 42.4%; p = 0.437). Analisi komorbiditas ( hipertensi, gagal ginjal, diabetes mellitus, dan obesitas) dan hasil angiografi ( jumlah pembuluh darah coroner yang sakit, diameter pembuluh darah, dan lokasi penyumbatan yang menyebabkan IMA-EST) tidak berhasil menunjukkan kemaknaan secara statistic. Kejadian efek samping sama pada kedua kelompok (21.6% vs. 15%). Kesimpulan: Pemberian kolkisin pada pasien IMA-EST yang menjalani IKPP tidak berhasil menurunkan kejadian cedera reperfusi. ......Background: Inflammation plays a role in ST-segment elevation myocardial infarction (STEMI), especially in reperfusion injury (RI). Colchicine, an anti-inflammatory drug, can suppress inflammation during RI. We assessed the effectiveness of administering colchicine to STEMI patients undergoing primary percutaneous coronary intervention (PPCI) in suppressing RI events. Methods: This study was a randomized, double-blind, placebo-controlled clinical trial conducted in a multicenter manner at two hospitals in Jakarta with IKPP facilities from December 2022 to April 2023. STEMI patients that underwent PPCI received 2 g of colchicine as a loading dose and a maintenance dose of 0.5 g every 12 hours for two days or amylum at a similar dose. Patients were observed for RI events (low-flow thrombolysis in myocardial infarction (0–2) during angiography procedure, reperfusion arrhythmia, cardiogenic shock, or persistent chest pain). Results: Seventy-seven STEMI patients with a mean age of 55.2 ± 9.9 years underwent PPCI. Of these patients, 37 received colchicine, and 40 received a placebo. Most subjects were male (77.5%), suffered three-vessel disease (44.15%), and occlusion in left anterior descending coronary artery (53.24%). Colchicine was found to fail to reduce the incidence of ischemia-RI (51.5% vs. 42.4%; p = 0.437). Analysis of comorbidities (hypertension, chronic kidney disease, diabetes mellitus, and obesity) and angiography results (vessel disease, lesion diameter, and culprit artery) failed to demonstrate a statistical difference in RI. Side effects were similar in the colchicine and placebo groups (21.6% vs. 15%). Conclusion: Colchicine administration in STEMI patients undergoing PPCI failed to reduce RI.

Abstrak :
Latar Belakang. Cedera Reperfusi-iskemik merupakan isu klinis yang penting dan umum. Hal tersebut dapat terjadi pada trombo-embolisme, penyakit vaskuler aterosklerotik, bedah kardiovaskuler, transplantasi organ, replantasi tungkai dll. Reperfusi jaringan yang iskemik bukan hanya menyebabkan reaksi iniamasi lokal tetapi juga mempengaruhi fungsi organ lain melalui respons inflamasi sistemik. Banyak studi menunjukkan sel polimorfonuklear terutama netrofil mempunyai peranan cedera yang panting dalam proses reperfusi-iskemik dengan menginfiltrasi jaringan iskemik dan juga kedalam organ yang jauh seperti hati, pare, ginjal dsb. Banyak obat yang sudah dicoba untuk untuk mengurangi efek cedera reperfusi dengan basil yang bervariasi. Salah satu obat yang menjanjikan dapat mengurangi cedera reperfusi melalui efek antiinflamasinya adalah Pentoksifilin (PTX). Pada studi eksperimental, kami mengamati efek pemberian PTX terhadap infiltrasi netrofil pada jaringan otot skeletal, hati dan pare hewan kelinci yang dibuat iskemik secara akut pada tungkai bawah dan diikuti dengan reperfusi. Metoda. Dua belas ekor kelinci jantan ras New Zealand White dibagi secara acak menjadi 3 grup (A,B dan C). Grup A diberikan PTX ( n=5); Group B diberikan NaCl 0.9% sebagai kontrol (n=5); Grup C adalah kontrol negatif (n=2). Grup A dan B mengalami total iskemia selama 3 jam pada tungkai bawah dengan Cara menjepit arteri iliaca komunis sinistra dengan klem. Dosis PTX adalah 40 mg/ kgBB bolus diikuti lmglkgBB sebagai dosis rumatan. PTX diberikan 30 menit sebelum reperfusi. Grup B diberikan NaCl 0.9 % dan pada grup C tidak dilakukan tindakan iskemia. Potongan jaringan histopatologi dari otot yang iakemik, hati dan pare diambil pada akhir percobaan (3jam setelah rep erfusi) sebelum dilakukan etanasia. Hasil. Jumlah rerata netrofil pada jaringan otot skeletal, hati dan pare berturut-turut adalah sebagai berikut : Pada grup C adalah 0.67 ± 0.75; 2.00 ± 1.41 dan 4.33 ± 1.49. GrupA adalah 3.53 ± 6.01; 7.20 ± 5.29 dan 13.87 t 7.84. Grup B adalah 13.80 ± 12.68; 12.33 ± 4.39 dan 34.13 ± 12.83. Tampak jumlah netrofil lebih rendah bermakna pada jaringan pare grup A dibandingkan grup B (p < 0.009). Ada kecenderungan jumlah netrofil lebih rendah dalam jaringan otot skeletal dan hati pada grup A dibandingkan grup B, walaupun secara statistik tidak bermakna (p < 0.075). Kesimpulan. Pentoksifilin dapat mempunyai efek mengurangi infiltrasi netrofil kedalam jaringan pada kelinci yang mengalami cedera reperfusi-iskemik tungkai akut.

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Background. Ischemic-reperfusion injury is a common and important clinical issues.lt occurs in many clinical setting such as thrombo-embolic phenonrenon,atherosclerotic vascular disease, cardiovascular surgery, organ transplantation, replantation of limb etc. Reperfusion of ischemic tissue not only causing local inflammatory reaction but also affect remote organ function by systemic-inflammatory responses. Many studies have showned that polymorphonuclear leukocyte especially neutrophil has an important damaging role in reperfusion injury. They exert their effect through infiltration into ischemic tissue and also into remote organ like liver,lung,kidney etc. So far a lot of agents have been tried to attenuate reperfusion injury with variable results. One promising drug for attenuating ischemic-reperfusion injury through its anti-inflammatory effect is Pentoxifylline (PTX). In this exploratory experimental study, we observed the effect of giving PTX on neutrophil infiltration to skeletal muscle, liver and lung tissue in rabbits with induced acute limb ischemia followed by reperfusion . Methods. Twelve male New Zealand White rabbits were randomly divided into 3 groups (A,B and C). Group A were given PTX(n =5); Group B using Na CI 0.9% as a control group (n= 5); Group C was negative control (n=2). Group A and B underwent 3 hours of total ischemia of the lower limb by clamping proximal left common iliac artery, follow by 3 hours of reperfusion. The dose of intravenous PTX was 40mg1kgB W bolus followed by 1 mg/kg BWlhour maintenance dose. PTX was given 30 minutes before reperfusion. Group B was given normal saline and in Group C, no intervention done. Histopathologic section of iskernic skeletal muscle, liver, and lung tissue were taken at the end of experiment before( 3 hours of reperfusion) euthanasia was done. Results. The mean numbers ofneutrophil in ischemic skeletal musle, liver and lung tissue consecutively were as follow ; In Group C were, 0.67 t 0.75; 2.00 f 1.41; and 4.33 ± 1.49. In group Awere,3.53 ±6.0]; 7.20±5.29; and 13.87±7,84, and in groupB (control)were 13.80 ± 12.68; 12.33 ± 4.39; and 34.13 ± 12.83. There was significantly lower number of netrophil in lung tissue of group A compare to group B (p< 0.009). Although not statistically significant (p= 0.075), there were a trend to have lower neutrophil counts in ischemic skeletal muscle and liver tissue in group A rabbits compared to group B. Conclusion. Pentoxifylline has attenuating effect on neutrophil infiltration in rabbits undergoing ischemic-reperfusion injury of lower limb.

Abstrak :
[ABSTRAK
Latar belakang : Pada masa sekarang, reperfusi miokardium dengan trombolitik atau intervensi koroner perkutan primer ( IKPP) adalah terapi utama pada pasien yang mengalami IMA EST. Tujuan utama IKPP untuk mengembalikan patensi arteri epikardial yang mengalami infark dan mencapai reperfusi mikrovaskular secepat mungkin. Namun keberhasilan mengembalikan patensi dari arteri koroner epikardial setelah oklusi tidak selalu menjamin cukupnya reperfusi ke level mikrovaskular, yang disebut sebagai fenomena no reflow atau microvascular obstruction (MVO). Terdapat dua mekanisme yang berperan pada no reflow yaitu disfungsi mikrovaskular dan kerusakan intergritas mikrostruktur endotel. Kerusakan endotel dapat diakibatkan berbagai hal, diantara nya jejas reperfusi yang akan mengaktivasi netrofil. Netrofil teraktivasi akan mengeluarkan radikal bebas oksigen, enzim proteolitik dan mediator proinflamasi yang secara langsung menyebabkan kerusakan jaringan dan endotel. Trimetazidine adalah obat antiangina yang dapat menurunkan netrofil yang dimediasi oleh trauma jaringan setelah jantung mengalami iskemia. Akan tetapi belum diketahui secara luas pengaruh pemberian trimetazidine terhadap akumulasi netrofil pada kejadian IMA EST yang dilakukan tindakan IKPP. Metode : Sebanyak 68 pasien IMA EST yang menjalani IKPP dipilih secara konsekutif sejak Januari 2015 sampai Juni 2015 diambil saat masuk UGD, dilakukan pengambilan darah vena perifer untuk menghitung jumlah netrofil sebelum IKPP, kemudian pasien menjalani IKPP. Setelah 6 jam paska IKPP dilakukan pengambilan kembali darah vena perifer untuk menghitung kembali jumlah netrofil paska IKPP. Hitung netrofil diperiksa dengan Sysmex 2000i. Perhitungan statistik dinilai dengan SPSS 17. Hasil : Dari 68 subyek, dibagi menjadi 28 subyek pada kelompok yang diberikan trimetazidine dan 40 subyek yang diberikan plasebo. Tidak didapatkan perbedaan jumlah netrofil pada kelompok perlakuan dan kelompok kontrol baik sebelum maupun sesudah IKPP, netrofil pre IKPP pada trimetazidine vs plasebo 10.71 ± 3.263 vs 10.99 ± 3.083,nilai p:0,341. Nilai netrofil post IKPP pada trimetazidine vs plasebo 9.49 ± 3.135 vs 9.92 ± 3.463,nilai p:0,664. Kesimpulan : Tidak terdapat penurunan jumlah netrofil pasca pemberian trimetazidine pada pasien IMA EST yang menjalani IKPP.

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ABSTRACT
Background Nowadays, reperfusion strategy, either with thrombolytic or Primary Percutaneous Coronary Intervention (PPCI), is the core treatment for Acute ST-Segment Elevation Myocardial Infarct (STEMI). The goal of PPCI is to restore the patency of infarcted epicardial artery and establish microvascular reperfusion as soon as possible so that necrotic myocardial area can be reduced. However, successful restoration of infarcted epicardial artery is not always followed by enough reperfusion to the microvascular part. Trimetazidine is an antianginal drug, can reduce neutrophil which was mediated by tissue trauma during ischemic heart condition. Trimetazidine is currently approved and widely known as antianginal drug which affect metabolism. Unfortunately, its influence over neutrophil accumulation in acute STEMI patients which undergo PPCI is not well understood. Method There were 68 consecutive-selected acute STEMI patients which undergo PPCI since January 2015 until Juni 2015. They were admitted in emergency department. Peripheral vein blood sampling was taken to measure neutrophil before PPCI was performed. Six hour after PPCI was conducted, another peripheral vein blood sampling was taken for another neutrophil measurement. Neutrophil measurement was performed with Sysmex 2000i. Statistical analysis was performed by using SPSS 17. Result Among 68 patients, divided in two groups, trimetazidine 28 patients and plasebo 40 patients. There were no differences amount of neutrophils in trimetazidine or plasebo group, before or after PPCI. Neutrophil pre PPCI in trimetazidine vs plasebo group 10.71 ± 3.263 vs 10.99 ± 3.083, p:0,341. Neutrophil post PPCI in trimetazidine vs plasebo group 9.49 ± 3.135 vs 9.92 ± 3.463, p:0,664. Conclusion There were no reducing amount of neutrophils after trimetazidine was given in patients STEMI which underwent PPCI., Background Nowadays, reperfusion strategy, either with thrombolytic or Primary Percutaneous Coronary Intervention (PPCI), is the core treatment for Acute ST-Segment Elevation Myocardial Infarct (STEMI). The goal of PPCI is to restore the patency of infarcted epicardial artery and establish microvascular reperfusion as soon as possible so that necrotic myocardial area can be reduced. However, successful restoration of infarcted epicardial artery is not always followed by enough reperfusion to the microvascular part. Trimetazidine is an antianginal drug, can reduce neutrophil which was mediated by tissue trauma during ischemic heart condition. Trimetazidine is currently approved and widely known as antianginal drug which affect metabolism. Unfortunately, its influence over neutrophil accumulation in acute STEMI patients which undergo PPCI is not well understood. Method There were 68 consecutive-selected acute STEMI patients which undergo PPCI since January 2015 until Juni 2015. They were admitted in emergency department. Peripheral vein blood sampling was taken to measure neutrophil before PPCI was performed. Six hour after PPCI was conducted, another peripheral vein blood sampling was taken for another neutrophil measurement. Neutrophil measurement was performed with Sysmex 2000i. Statistical analysis was performed by using SPSS 17. Result Among 68 patients, divided in two groups, trimetazidine 28 patients and plasebo 40 patients. There were no differences amount of neutrophils in trimetazidine or plasebo group, before or after PPCI. Neutrophil pre PPCI in trimetazidine vs plasebo group 10.71 ± 3.263 vs 10.99 ± 3.083, p:0,341. Neutrophil post PPCI in trimetazidine vs plasebo group 9.49 ± 3.135 vs 9.92 ± 3.463, p:0,664. Conclusion There were no reducing amount of neutrophils after trimetazidine was given in patients STEMI which underwent PPCI.]

Abstrak :
Penyakit jantung koroner (PJK) atau penyakit jantung iskemik (infark miokard) merupakan salah satu penyebab utama kematian di seluruh dunia. Tindakan reperfusi miokardium merupakan tatalaksana utama PJK. Cedera iskemia-reperfusi (IRI) merupakan cedera lanjutan otot jantung akibat disfungsi seluler yang dapat terjadi setelah reperfusi. Transforming growth factor-beta (TGF-β) merupakan sitokin anti-inflamasi yang berperan dalam resolusi inflamasi dan inisiasi perbaikan infark, namun TGF-β juga mengaktivasi jalur fibrogenik yang menyebabkan fibrosis, hipertrofi dan percepatan gagal jantung. Kolkisin dosis rendah diketahui menurunkan ekspresi TGF-β. Penelitian ini bertujuan menilai pengaruh pemberian kolkisin terhadap perubahan kadar TGF-β pada serum pasien infark miokard akut-elevasi segmen ST (IMA-EST) sebelum dan pada 48 jam pasca tindakan reperfusi. Penelitian dilakukan menggunakan desain uji klinik tersamar ganda (double blinded randomized clinical trial) yang melibatkan 64 subjek. Pada hasil penelitian didapatkan peningkatan kadar TGF-β yang lebih tinggi pada 48 jam pasca reperfusi, terutama pada kelompok studi. Tidak didapatkan perbedaan bermakna pada analisis perubahan (delta) kadar TGF-β sebelum dan pada 48 jam pasca tindakan reperfusi antara kedua kelompok. Penelitian ini merupakan penelitian pertama yang menilai pengaruh pemberian kolkisin terhadap kadar TGF-β pada pasien IMA-EST pasca reperfusi. Penelitian ini dapat dijadikan dasar penelitian lanjutan untuk menilai perubahan kadar TGF-β dengan pemberian kolkisin dalam jangka panjang. ......Coronary heart disease or ischemic heart disease (myocardial infarction) is one of the leading causes of death worldwide. The primary management for CHD is myocardial reperfusion. Ischemia-reperfusion injury is a type of secondary cardiac muscle injury induced by cellular dysfunction following reperfusion. Transforming growth factor-beta (TGF-β) is an anti-inflammatory cytokine that aids in inflammatory resolution and initiation of infarct healing, but it also stimulates fibrogenic pathways that promote fibrosis, hypertrophy and accelerated heart failure. Low doses of colchicine have been shown to inhibit TGF-β expression. The purpose of this study is to see how colchicine affects TGF-β serum levels in patients with acute ST-segment elevation myocardial infarction (IMA-EST) before and 48 hours after reperfusion. This study used a double blinded randomized clinical trial design involving 64 subjects. This study’s findings revealed a larger increase in TGF-β levels 48 hours after reperfusion, particularly in the study group. There was no significant difference in TGF-β level changes before and 48 hours after reperfusion between the two groups. This is the first study to evaluate the effect of colchicine on TGF-β levels in IMA-EST patients and can be used to guide future research into the effects of long-term colchicine administration on TGF-β levels

Abstrak :
Latar Belakang:Banyak penelitian telah membuktikan pengaruh faktor inflamasi terhadap sindroma koroner akut.Tingginya jumlah leukosit pasca intervensi koroner perkutan primer (IKPP) menggambarkan respon inflamasi pada patofisiologi infark miokard akut dengan elevasi segmen ST (IMA – EST)dan respon terhadap kerusakan dinding arteri.Hal ini dihubungkan dengan luaran klinis yang buruk.Tujuan penelitian ini adalah untuk menilai pengaruh jumlah leukosit pasca IKPP terhadap perbaikan fungsi jantung kiri menggunakan indeks gerakan otot jantung segmental (RWMI) pada area terkait infark. Metode:Sebanyak 62 subjek IMA–EST yang menjalani IKPP secara konsekutif dipilih dan diikuti selama 30 hari, sejak 1 Januari–30 April 2013. Jumlah hitung leukosit diukur pada saat masuk dan 48 jam pasca IKPP, derajat sebukan miokard (MBG), aliran TIMI dan RWMI diukur segera setelah IKPP. RWMI dievaluasi menggunakan ekokardiografi setelah 30 hari pasca infark, dengan menilai kesepahaman intra dan inter observer. Perhitungan statistik dinilai dengan software stata versi 12. Hasil: Pasien dengan jumlah leukosit 48 jam pasca IKPP > 12,020/uL memiliki OR: 4,4 (95% CI: 0,98 – 19,85; p = 0,05) untuk mengalami irreversibilitas gerakan otot jantung segmental terkait infark pada 30 hari, analisa multivariat menunjukan leukosit pasca IKPP secara konsisten memprediksi irreversibilitas RWMI dengan OR 5,6 (95% CI: 1,08 – 28,6; p = 0,039). Kesimpulan: Jumlah leukosit pasca IKPP diatas quartile ke-3 dengan lebih dari 12,020/uL pada jam ke-48 dapat meningkatkan risiko irreversibilitas gerakan otot jantung segmental ventrikel kiri, pada area terkait infark pasien IMA-EST. ......Background: Many researches has proven inflammation response in the pathophysiology of acute coronary syndrome (ACS) with ST segment elevation (STEMI). High leukocyte count post primary percutaneous intervention (PPCI) describes the magnitude of inflammatory state in ACS and inflammatory respond to arterial injury, and associated with poor prognosis. The aim of this study was to see the correlation between leucocytes post PPCI with improvement of left ventricle function measure by regional wall motion index (RWMI). Method: 62 STEMI subjectswhom underwent PPCI were selected consecutively between 1st Jan – 30th Apr 2013, and followed up for 30 days. Total leukocyte count was measure during admission and 48 hours post PPCI. TIMI flow and myocardial blush grade were measure immediately post procedural. RWMI was measure soon after PPCI and at 30 days, intra and inter observer variability were analyzed. Logistic regression was used to correlate variable independent and dependent, using software Stata version 12. Result: Patients with 48 hours leukocyte count >12,020/uL post PPCI, has OR 4,4 (95% CI: 0,98 – 19,85; p = 0,05), to predict irreversibility in regional systolic wall motion related to infarct teritory,measure at 30 days.Multivariate analysis consistently shown leukocyte post PPCI as strong predictor of RWMI irreversibility, with OR 5,6 (95% CI: 1,08 – 28,6; p = 0,039). Conclusion: High total leukocyte count post PPCI above 3rd quartile, > 12,020/uL taken at 48 hours,increase the risk of regional wall motion irreversibility in infarct related area.

Abstrak :
Pendahuluan. Cedera iskemia reperfusi CI/R merupakan fenomena kerusakan selular akibat hipoksia yang terjadi lebih hebat saat restorasi oksigen. Strangulasi usus merupakan kasus bedah tersering yang dapat menimbulkan CI/R pada hati sebagai organ yang langsung mendapatkan aliran darah dari usus. Tindakan destrangulasi dalam mengembalikan perfusi oksigen dan menilai viabilitas usus yang dilakukan intraoperatif dapat menimbulkan CI/R terutama pada kasus dimana kemungkinan besar usus akan dilakukan reseksi. Studi ini bertujuan untuk mengetahui pengaruh destrangulasi usus pada kasus strangulasi usus terhadap hati. Metode. Studi eksperimental pada tikus Sprague ndash;Dawley dengan membandingkan kadar Serum Glutamic Oxaloacetic Transaminase SGOT , Serum Glutamic Pyruvic Transaminase SGPT , malondialdehyde MDA serum dan hati serta histopatologi derajat kerusakan hati pada kelompok perlakuan reseksi usus dengan destrangulasi D dan tanpa destrangulasi TD setelah dilakukan strangulasi usus selama 4 jam. Hasil. Tidak terdapat perbedaan kadar SGOT p=0.234 , SGPT p=0.458 , MDA serum p=0.646 dan MDA hati p=0.237 antara kontrol, kelompok D dan TD. Pada histopatologi derajat kerusakan hati terdapat perbedaan bermakna antara kontrol dengan kedua kelompok perlakuan p=0.006 , namun tidak didapatkan perbedaan bermakna antara kelompok D dan TD p=0.902. Kesimpulan. Tindakan destrangulasi sebelum reseksi pada kasus strangulasi usus tidak menimbulkan perbedaan kadar biomarker stress oksidatif dan derajat kerusakan hati dibandingkan dengan tanpa destrangulasi. ...... Introduction. Ischaemia-reperfusion injury IRI is cellular injury due to hypoxia with greater impact when oxygen restored. Intestinal strangulation are often in surgical emergency that cause IRI on liver that directly get blood from intestine. Destrangulation that performed intraoperatively as purposes to restored oxygen and to evaluate viability of intestine tissue, can cause IRI particularly on case with partly of intestine will be resected. This study is to investigate intestinal destrangulation effects on liver following intestinal IRI. Method. This is an experimental study using Sprague-Dawley to compare Aspartate Aminotransferase AST, Alanine Aminotransferase ALT, serum and liver malondialdehyde MDA, and histopathology of degree liver injury between group of resection following destrangulation D and without destrangulation WD after 4 hours strangulation of one loop intestine. Results. There were no significant difference on AST p=0.234, ALT p=0.458, serum MDA p=0.646 and liver MDA p=0.237 between control, D and WD group. Histopathology examination showed significant difference between control and both of treatment group p=0.006, but there was no significant difference between D and WD group p=0.902. Conclusion. Destrangulation before resection on the intestinal strangulation cases doesn rsquo;t cause different of oxidative stress biomarker level and degree of liver injury, compare to intestinal resection without destrangulation.

Abstrak :
Much has been written about reperfusion injury in the past decade but unfortunately the information has been generally presented in the form of original specialist papers and little if any integral publication exists on the topic, summarising and analysing the clinical impact of the condition and its management. The pathophysiology and molecular mechanisms of reperfusion injury are complex and, regarding diagnosis, individual diagnostic techniques have been proposed but without a proper assessment of the relative values of these methods. A publication dealing with integral diagnostic strategies would be welcome by the managing physician. Management of the condition is also problematic, as strategies that appear to work in the experimental models do not translate into beneficial interventions in patients. There is a need for these issues to be addressed and discussed in a monographic fashion. Management of myocardial reperfusion injury will tackle these issues in a modern and systematic way and the information will be delivered in a fashion that will be appealing to the reader.

Abstrak :
Pengaruh Prekondisi dan Hipotermia pada Cedera Iskemia-Reperfusi Terhadap Endotel Pembuluh Darah Perifer pada Oryctolagus cuniculusM Febriadi Ismet1 Yefta Moenadjat2 Aria Kekalih3 1Program Studi Ilmu Bedah, Fakultas Kedokteran Universitas Indonesia2Departemen Medik Ilmu Bedah, RSUPN Cipto Mangunkusumo Pendahuluan. Cedera iskemia -reperfusi CI/R merupakan masalah serius yang dihadapi pascahipoksia; menyebabkan kerusakan sel yang letaknya remote organ injury. Intervensi prekondisi iskemia-reperfusi PI/R merupakan fenomena jaringan yang diberikan stimulasi hipoksia berulang sebelum mendapatkan keadaan iskemia lama. Keadaan hipotermia iskemia reperfusi HI/R menyebabkan metabolisme sel menurun termasuk respon sel terhadap iskemia. Penelitian ini bertujuan untuk mengetahui efek intervensi PI/R dan HI/R terhadap perubahan morfologi endotel pembuluh darah dan peningkatan kadar malondialdehyde MDA sebagai respon stress oksidatif pada jaringan endotel a/v femoralis komunis distal obstruksi iskemia dan kontralateral CI/R. Metode: Studi eksperimental yang bersifat deskriptif analitik pada Oryctolagus cuniculus, Pada kelompok CI/R dilakukan ligasi arteri femoralis komunis dalam pembiusan selama empat jam untuk menginduksi iskemia. Pada kelompok PI/R dilakukan dengan ligasi berulang arteri femoralis komunis kanan selama dua menit, dilepaskan tiga menit sebanyak dua siklus, kemudian diligasi selama empat jam. Pada kelompok hipotermia, dilakukan ligasi arteri femoralis komunis selama empat jam yang disertai dengan membungkus ekstremitas bawah kanan dengan es dengan target suhu antara 31-33 C, kemudian pada ketiga intervensi ligasi dibuka dan kelinci dibiarkan beraktivitas selama delapan jam. Setelah itu, dilakukan pengambilan sampel a.v yang berasal dari distal dari ligasi ipsilateral dan kontralateral untuk pemeriksaan histopatologi dan biokimia. Pemeriksaan biokimia dilakukan menggunakan malondialdehid MDA. Hasil: Pada pemeriksaan histomorfologi menunjukan perbedaan bermakna antara skoring kerusakan endotel jaringan a.v. ipsilateral pada ketiga sampel intervensi dibanding kontrol dan nilai sampel intervensi preventif lebih baik daripada sampel CI/R p< 0,05 . Pada sampel a.v kontralateral kelompok PI/R dan HIR tidak memiliki perbedaan bermakna dengan kontrol p> 0,05 . Pada evaluasi kadar MDA ditemukan kadar MDA meningkat pada semua intervensi baik pada CIR, PI/R, dan HI/R yang tidak berbeda bermakna dengan kontrol p> 0,05. Konklusi: Keadaan CI/R menyebabkan disfungsi endotel bukan hanya pada daerah iskemik, namun pada organ yang letaknya berjauhan. Kerusakan endhotelial lining dapat dicegah dengan tindakan PI/R dan HI/R dan peningkatan kadar MDA merupakan respon fisiologis jaringan terhadap iskemia dan cedera reperfusi yang terjadi baik pada CI/R, PI/R, dan HI/R. ...... The Effect of Preconditioning and Hypothermia in Ischemia Reperfusion Injury to the Endothelial Cells from Peripheral Blood Vessels in Oryctolagus cuniculusM Febriadi Ismet1 Yefta Moenadjat2 Aria Kekalih31General Surgery Science Study Program, Faculty of Medicine Universitas Indonesia2Department of Surgery, Dr. Cipto Mangunkusumo National General HospitalIntroduction. Ischemia reperfusion injury IRI is a serious problem in the post hypoxia period, which causes remote organ injury. Ischemic preconditioning IPC is a phenomenon where tissues are subjected to repeated hypoxic stimulations to protect against subsequent prolonged period of ischemia. Hypothermia during ischemia reperfusion injury HI decreases metabolism of cells including their response to ischemia. The goal of this study is to investigate the effects of interventions such as IPC and HI on the morphology of endothelial cells in blood vessels and the increased level of malondialdehyde MDA as an oxidative stress response in endothelial tissues of distal common femoral artery and vein obstruction ischemia and its contralateral IRI. Method: This is a descriptive and analytic experimental study using Oryctolagus cuniculus. In the IRI group, the common femoral artery was ligated during anesthesia for four hours to induce ischemia. In the IPC group, the right common femoral artery was continually ligated for two minutes, which was then released for three minutes for two cycles, and then ligated for four hours. In the hypothermia group, the common femoral artery was ligated for four hours and the right lower extremity was wrapped in ice with the target temperature range between 31 33o C. Then the arteries from the three interventions were unligated and the rabbit was released to observe its activity for eight hours. Next, samples of artery and vein distal from the ligation ipsilateral and its contralateral were obtained for histopathological and biochemical examinations. The biochemical analysis was performed using malondialdehyde MDA. Results: The histomorphological examination showed significant difference in the injury scores between the endothelial tissues from ipsilateral artery and vein in the three interventional samples compared with control, and the scores for the preventive intervention groups were better than the IRI sample p0.05. Conclusion: Ischemic reperfusion injury can cause not only endothelial dysfunction in the ischemic area, but also remote organ injury. Endothelial lining injury can be prevented by IPC and HI. The elevated level of MDA is a physiological response of tissue after ischemia reperfusion injury which could be found on IRI, IPC, and HI.