The possible involvement of platelet activation in endotoxin-induced renal insufficiency in a rabbit model.

M Yokota, J Kambayashi, M Sakon, H Tahara, E Shiba, T Kawasaki, T Mori
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引用次数: 1

Abstract

The effects of the anticoagulants, heparin and low molecular weight heparin (LMWH), and the antiplatelet agents, prostaglandin E1 (PGE1) and aspirin, on endotoxin-induced renal insufficiency not induced by prerenal factors, were investigated using rabbits to evaluate the clinical usefulness of these drugs and their possible involvement in the activation of hemostasis in renal insufficiency. The intravenous administration of PEG1, at 0.4 microgram/kg/min, or aspirin, at 5 mg/kg, significantly restored all the parameters of renal function measured in the present study, namely, effective renal plasma flow, glomerular filtration rate and urine N-acetyl-beta-D-glucosaminidase, as well as histological renal ischemic changes. On the other hand, neither heparin nor LMWH, even at a high dose, improved any parameter. As the antiplatelet effect is the common property of PGE1 and aspirin, it is suggested that the activation of platelets may be prerequisite to the occurrence of renal insufficiency induced by endotoxin. The results of this study thus show that PGE1 or aspirin may be applied in clinical use for renal insufficiency complicated by sepsis or endotoxemia.

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兔内毒素致肾功能不全模型中血小板活化的可能参与。
采用家兔研究抗凝剂肝素、低分子肝素(LMWH)及抗血小板药物前列腺素E1 (PGE1)、阿司匹林对非肾源性内毒素性肾功能不全的影响,探讨其临床应用价值及可能参与肾功能不全的止血作用。静脉给药PEG1(0.4微克/千克/分钟)或阿司匹林(5毫克/千克)可显著恢复本研究测量的所有肾功能参数,即有效肾血浆流量、肾小球滤过率和尿n -乙酰- β - d -氨基葡萄糖苷酶,以及肾缺血组织学改变。另一方面,肝素和低分子肝素,即使在高剂量下,也没有改善任何参数。抗血小板作用是PGE1和阿司匹林的共同特性,提示血小板活化可能是内毒素引起肾功能不全发生的前提。因此,本研究结果表明PGE1或阿司匹林可用于临床治疗肾功能不全合并脓毒症或内毒素血症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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