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"Panduan resusitasi anak umumnya menganjurkan pemberian cairan dalam jumlah besar. Beberapa penelitian memperlihatkan bahwa penggunaan cairan yang agresif meningkatkan mortalitas. Penelitian pada hewan menunjukkan tekanan vena sentral yang tinggi memicu pelepasan atrial natriuretic peptide ANP , sementara penelitian invitro memperlihatkan ANP meluruhkan glycocalyx endotel vaskular dan meningkatkan permeabilitas endotel. ANP juga memicu vasodilatasi. Hemodilusi berpotensi menurunkan pasokan oksigen tubuh DO2 . Penelitian bertujuan untuk melihat pengaruh resusitasi cairan terhadap kadar ANP serum, peluruhan glycocalyx endotel vaskular, extravascular lung water index ELWI , mean arterial pressure MAP , kadar hemoglobin dan pasokan oksigen. Hewan model renjatan adalah 11 ekor Sus scrofa jantan, usia 6-10 minggu. Renjatan dilakukan dengan metode fixed pressure hemorrhage. Resusitasi pertama dilakukan dengan jumlah cairan sesuai darah yang dikeluarkan resusitasi normovolemik , dilanjutkan dengan 40 mL/kg resusitasi hipervolemik . Pengukuran hemodinamik dilakukan dengan PICCO. Serum ANP dan Syndecan-1, petanda peluruhan glycocalyx, dilakukan dengan teknik ELISA. Hasil penelitian menunjukkan terjadinya peningkatan ANP pasca resusitasi normovolemik p = 0,043 , yang kemudian menurun kembali dalam 30 menit. Peluruhan glycocalyx tidak terjadi. Perbedaan ELWI pada 60 menit pasca resusitasi secara statistik bermakna, dengan perbedaan 0,93 mL/kg 95 IK:0,19 -3,62 . Terdapat korelasi kuat antara SVRI dan CI pasca resusitasi hipervolemik r = -0,587 . Tidak ada perbedaan MAP pasca resusitasi normovolemik dan hipervolemik. Kadar hemoglobin pasca resusitasi hipervolemik lebih rendah daripada pasca resusitasi normovolemik p = 0,009 . Pasokan oksigen tubuh pasca resusitasi hipervolemik lebih tinggi daripada pasca resusitasi normovolemik p = 0,012 . Simpulan: Resusitasi cairan pada renjatan akibat perdarahan tidak mengakibatkan peluruhan glycocalyx endotel vaskular. Peningkatan ELWI amat terbatas. SVRI berkorelasi terbalik dengan CI. Tidak ada perbedaan MAP antara resusitasi normovolemik dan hipervolemik. Resusitasi hipervolemik menyebabkan hemodilusi yang diimbangi dengan peningkatan curah jantung.

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Many pediatric guidelines recommend liberal fluid resuscitation, but recent studies showed that aggressive fluid resuscitation might increase mortality. Animal studies showed that high central venous pressure induced ANP secretion. Invitro studies showed convincing evidence that ANP induced glycocalyx shedding. ANP also induced vasodilatation through cGMP signal transduction pathways. Hemodilution due to a large amount of resuscitation fluid potentially decreasing oxygen delivery.The objectives of this study were investigating the effect of fluid resuscitation, in the animal model, with special concern on serum ANP, glycocalyx shedding indicate by serum Syndecan-1 , changes in extravascular lung water, systemic vascular resirtance and mean arterial pressure, hemoglobin level and oxygen delivery DO2 . The animal models were 11 male domestic pigs, 6 -10 weeks old. The shock was induced with fixed pressure hemorrhage method. Fluid resuscitation was done in 2 phases. On the first attempt, we replaced total numbers of blood that withdrawn normovolemic resuscitation . On the second attempt, we gave 40 mL/kg resuscitation fluids hypervolemic resuscitation . The hemodynamic measurements were done with PICCO. Serum ANP and Syndecan-1 were measure with ELISA method.We found that serum ANP increased after normovolemic resuscitation p = 0.043 and immediately back to base level in 30 minutes. Glycocalyx shedding did not occur. Extravascular lung water index minimally increased. There was a strong correlation between SVRI and CI at hypervolemic resuscitation r = -0.587 . There was no difference in mean arterial pressure between normovolemic and hypervolemic resuscitation. Hemoglobin level after hypervolemic resuscitation was lower than after normovolemic resuscitation p = 0.009 . Oxygen delivery was higher after hypervolemic resuscitation p = 0.012 .Conclusions: Hypervolemic resuscitation in this hemorrhagic shock model did not induce glycocalyx shedding, extravascular lung water index minimally increased. Systemic vascular resistance index negatively correlated to cardiac index. Fluid resuscitation may induce hemodilution, but oxygen delivery can be compensated by increasing cardiac output. "

"Lupus eritematosus sistemik merupakan penyakit autoimun sistemik yang menghasilkan berbagai autoantibodi yang ditujukan terhadap komponen sel, seperti inti sel, sitoplasma dan membran sel. Salah satu autoantibodi tersebut yaitu antibodi anti ?2GP-1 dihubungkan dengan kejadian aterosklerosis dan penyakit kardiovaskular yang timbul lebih dini pada pasien SLE. Penelitian ini bertujuan untuk mengetahui hubungan antibodi anti ?2GP-1 dengan disfungsi endotel dan aterosklerosis pada pasien SLE dan disfungsi endotel pada HUVEC. Penelitian potong lintang pada pasien SLE yang memenuhi kriteria inklusi menurut ACR 1997 di poliklinik khusus Reumatologi, Alergi Imunologi RSCM dan poliklinik khusus Reumatologi RSUP Dr. M. Djamil dari Maret 2016 sampai dengan Juli 2017. Subjek secara acak dibagi atas 2 kelompok berdasarkan nilai CIMT. Dilakukan pemeriksaan antibodi anti ?2GP-1, ox-LDL, ADMA, ICAM-1, VCAM-1, ET-1. Dilakukan pemajanan antibodi anti ?2GP-1 yang berasal dari kelompok aterosklerosis positif dan kontrol pada HUVEC. Enam puluh enam orang subjek direkrut pada penelitian ini, terdiri atas 33 orang aterosklerosis positif dan 33 orang aterosklerosis negatif dan 6 orang kontrol dengan rentang umur 20-45 tahun. Ditemukan korelasi positif antara antibodi anti ?2GP-1 dengan CIMT,ADMA, ICAM-1, VCAM-1 dan ET-1 dengan nilai r = 0,409, 0,89, 0,36, 0,43, 0,37 dan dengan p < 0,05. Tidak ditemukan korelasi antibodi anti ?2GP-1 dengan ox-LDL dengan r = 0,025 dan p > 0,05. Ditemukan perbedaan bermakna kadar antibodi anti ?2GP-1, ADMA, ICAM-1, VCAM-1 dan ET-1 pada kelompok aterosklerosis positif dengan kelompok aterosklerosis negatif dengan nilai p < 0,05, sedangkan kadar ox-LDL tidak ada perbedaan bermakna pada kedua kelompok tersebut dengan nilai p > 0,05. Hasil pemajanan antibodi anti ?2GP-1 pada HUVEC mendapatkan perbedaan bermakna peningkatan kadar ICAM-1, VCAM-1 dan ET-1 pada kelompok SLE aterosklerosis positif dari kontrol dengan nilai p < 0,05. Antibodi anti ?2GP-1 menimbulkan disfungsi endotel pada pasien SLE.

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Systemic lupus erythematosus SLE is a multi systemic disease characterized by a wide variety of autoantibodies directed to several self molecules found in the nucleus, cytoplasm and cell membrane. One of variety autoantibodies is Antibody anti 2GP 1 which associated with atherosclerosis and premature cardiovascular disease in SLE patients. The purpose of the study is to know the association of antibody anti 2GP 1 with endothelial dysfunction and atherosclerosis in SLE and endothelial dysfunction in HUVEC. Cross sectional study was performed in SLE patients fulfill inclussion criteria according ACR 1997 out patients in Rheumatology and Alergy Immunology polyclinic of Cipto Mangunkusomo Hospital and Dr. M. Djamil Hospital from March 2016 to July 2017. Patients were divided in 2 groups based on CIMT. Examination of antibody anti 2GP 1, ox LDL, ADMA, ICAM 1, VCAM 1 and ET 1 were performed. Purified antibody anti 2GP 1 from positive atherosclerosis and controls groups were exposed to HUVEC. Sixty six patients were enrolled, consists of 33 patients with positive atherosclerosis, 33 patients with negative atherosclerosis and 6 as healthy control with range of age 20 40 year. In this study we found positive correlation between antibody anti 2GP 1 with CIMT, ADMA, ICAM 1, VCAM 1 and ET 1 with r 0.409, 0.89, 0.36, 0.43, 0.43 respectively and p value 0.05. There was no correlation between antibody anti 2GP 1 with ox LDL, r 0.025 and p 0.05. There were significantly different levels of antibody anti 2GP 1, ADMA, ICAM 1, VCAM 1 and ET 1 in positive atherosclerosis compared to negative atherosclerosis group with p 0.05. Level of ox LDL was not different between the two groups with p 0.05. There were significantly different increase of ICAM 1, VCAM 1 and ET 1 levels in HUVEC which was exposed with purified antibody anti 2GP 1 from positive atherosclerosis compared to control with p 0.05. Antibody anti 2GP 1 cause endothelial dysfunction in SLE patients. "