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内皮素抗体或SB 209670对内毒素诱导的肾衰竭无效。

Lack of effect of ET antibody or SB 209670 on endotoxin-induced renal failure.

作者信息

Wellings R P, Corder R, Vane J R

机构信息

William Harvey Research Institute, St. Bartholomew's Hospital Medical College, London, England.

出版信息

J Cardiovasc Pharmacol. 1995;26 Suppl 3:S476-8.

PMID:8587451
Abstract

Elevated plasma levels of endothelin-1 (ET-1) in patients with septic shock have implicated ET-1 in the vascular hypoperfusion and organ dysfunction, including renal failure, that occur in this condition. Administration of endotoxin to rats induces renal dysfunction characterized by increased blood urea nitrogen (BUN) and plasma creatinine (Cr) levels. Here, we have found that neither SB 209670 (an ETA and ETB receptor antagonist) nor an affinity-purified ET antibody blocked the endotoxin-induced changes in renal function, suggesting that ET-1 is not involved in the pathophysiology of endotoxin-induced renal dysfunction.

摘要

脓毒性休克患者血浆中内皮素-1(ET-1)水平升高,这表明ET-1与该病症中出现的血管灌注不足及包括肾衰竭在内的器官功能障碍有关。给大鼠注射内毒素会诱发以血尿素氮(BUN)和血浆肌酐(Cr)水平升高为特征的肾功能障碍。在此,我们发现SB 209670(一种ETA和ETB受体拮抗剂)及亲和纯化的ET抗体均不能阻断内毒素诱导的肾功能变化,这表明ET-1不参与内毒素诱导的肾功能障碍的病理生理学过程。

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