受体阻滞剂品多洛尔对HgCl2诱导的犬急性肾功能衰竭存活的影响。

J Siklós, K Gaál
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引用次数: 0

摘要

研究了受体阻滞剂品多洛尔对HgCl2中毒犬存活的影响。对照犬单次静脉注射100微克/kg b.w.品多洛尔,尿钠排泄量显著升高,血浆肾素活性(PRA)和尿去甲肾上腺素(NE)、肾上腺素(E)排泄量显著降低。单次注射3mg /kg HgCl2静脉注射,动物在3-5天内死亡。用上述剂量的品多洛尔预处理后,存活时间延长了4 ~ 8天,2只狗从急性肾功能衰竭(ARF)中恢复。预处理组氮血症的程度小于只给予HgCl2的对照组。品多洛尔阻止盐酸引起的尿儿茶酚胺排泄和PRA的显著增加。这些发现支持了交感神经系统活动增加参与ARF肾毒性模型病理机制的假设。品多洛尔预处理虽不能预防ARF,但可降低ARF的严重程度。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of the beta-receptor blocker pindolol on survival in HgCl2 induced acute renal failure in dogs.

The effect of the beta receptor blocker pindolol on survival was investigated in HgCl2 intoxicated dogs. A single injection of 100 microgram/kg b.w. pindolol intravenously (i.v.) caused a significant rise in urinary sodium excretion and a significant decrease of plasma renin activity (PRA) and urinary norepinephrine (NE) and epinephrine (E) excretion in control dogs. A single injection of 3 mg/kg HgCl2 i.v. resulted in death of the animals within 3-5 days. Pretreatment with the above dose of pindolol increased length of survival 4-8 days, two dogs recovering from acute renal failure (ARF). The degree of azotemia was smaller in the pretreated group than in the control dogs given HgCl2 only. Pindolol prevented the HgCl2 induced marked increases of urinary catecholamine excretion and PRA. These findings support the hypothesis that increased activity of the sympathetic nervous system is involved in the pathomechanism of the nephrotoxic model of ARF. Pindolol pretreatment decreases the severity of ARF though it can not prevent it.

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