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[大鼠常温缺血再灌注所致肝损伤。己酮可可碱预处理的影响]

[Liver damage due to normothermic ischemia and reperfusion in the rat. The effects of pentoxifylline pretreatment].

作者信息

Ratia Giménez T, Navidad Novalvos R, Martínez Onturbe P, Santamaría Solís L V, Castillo Olivares Ramos J L

机构信息

Servicio de Cirugía Experimental, Clínica Puerta de Hierro, Madrid.

出版信息

Rev Esp Enferm Dig. 1995 Jul;87(7):509-15.

PMID:7662419
Abstract

The effect of pretreatment with pentoxifylline on normothermic liver ischemia was studied in rats. This drug, a dimethylxanthine and fosfodiesterase inhibitor, improves microcirculation, decreases neutrophil activity in experimental sepsis and hemorrhagic shock, and inhibits "in vitro" cytokine production by isolated Kupffer cells. Partial liver ischemia was induced by occlusion of afferent vessels to the median and left lateral lobes for 60', followed by resection of nonischemic lobes just before reperfusion. The rats were divided in 4 groups: I (n = 6) sham operation, II (n = 6) resection of right and caudate lobes, III (n = 42) normal saline pretreatment and 60' ischemia, IV (n = 42) pentoxyfilline pretreatment (50mg/K/i.p. 2 h before clamping) and 60' ischemia. 12 animals were sacrificed 1 h and 6 h after reperfusion respectively (gr III and IV), and 20 rats were observed for a maximum of 24 h after reperfusion. Serum transaminases, LDH, CK (isoenzymes), bilirubin, and total bile acids were determined in each animal. A sample of the left lobe was taken for histological examination. Extent of necrosis 24 h after reperfusion was assessed. Bile output was measured before ischemia and during the first hour of reperfusion. Pentoxifylline pretreatment was associated with a lower rise in serum transaminases and LDH after reperfusion, but it did not modify the changes in either serum CK activity (mainly CKBB), or total bile acid concentration. A reduction of bile output was not avoided by pentoxifylline pretreatment.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在大鼠中研究了己酮可可碱预处理对常温肝缺血的影响。这种药物是一种二甲基黄嘌呤和磷酸二酯酶抑制剂,可改善微循环,降低实验性脓毒症和失血性休克时的中性粒细胞活性,并抑制分离的库普弗细胞“体外”细胞因子的产生。通过阻断中叶和左外叶的输入血管60分钟诱导部分肝缺血,然后在再灌注前切除非缺血叶。将大鼠分为4组:I组(n = 6)假手术,II组(n = 6)切除右叶和尾状叶,III组(n = 42)生理盐水预处理并缺血60分钟,IV组(n = 42)己酮可可碱预处理(夹闭前2小时腹腔注射50mg/K)并缺血60分钟。分别在再灌注后1小时和6小时处死12只动物(III组和IV组),20只大鼠在再灌注后最多观察24小时。测定每只动物的血清转氨酶、乳酸脱氢酶、肌酸激酶(同工酶)、胆红素和总胆汁酸。取左叶样本进行组织学检查。评估再灌注24小时后的坏死程度。在缺血前和再灌注的第一小时测量胆汁分泌量。己酮可可碱预处理与再灌注后血清转氨酶和乳酸脱氢酶的较低升高有关,但它并未改变血清肌酸激酶活性(主要是CKBB)或总胆汁酸浓度的变化。己酮可可碱预处理未能避免胆汁分泌量的减少。(摘要截短于250字)

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Rev Esp Enferm Dig. 1995 Jul;87(7):509-15.
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