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血小板活化在兔模型内毒素诱导的肾功能不全中的可能作用。

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

作者信息

Yokota M, Kambayashi J, Sakon M, Tahara H, Shiba E, Kawasaki T, Mori T

机构信息

Second Department of Surgery, Osaka University Medical School, Japan.

出版信息

Jpn J Surg. 1991 Sep;21(5):542-6. doi: 10.1007/BF02470992.

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.

摘要

使用兔子研究了抗凝剂肝素和低分子量肝素(LMWH)以及抗血小板药物前列腺素E1(PGE1)和阿司匹林对非肾前因素引起的内毒素诱导的肾功能不全的影响,以评估这些药物的临床实用性及其在肾功能不全中可能参与的止血激活作用。以0.4微克/千克/分钟的剂量静脉注射PGE1或5毫克/千克的阿司匹林,可显著恢复本研究中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,以及肾脏组织学缺血变化。另一方面,即使高剂量的肝素和LMWH也不能改善任何参数。由于抗血小板作用是PGE1和阿司匹林的共同特性,提示血小板活化可能是内毒素诱导的肾功能不全发生的先决条件。因此,本研究结果表明,PGE1或阿司匹林可用于临床治疗并发败血症或内毒素血症的肾功能不全。

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