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普萘洛尔预处理预防犬内毒素诱导的脑氧消耗增加。

Prevention of endotoxin-induced increase of cerebral oxygen consumption in dogs by propranolol pretreatment.

作者信息

Westerlind A, Larsson L E, Häggendal J, Ekström-Jodal B

机构信息

Department of Anaesthesiology, Sahlgren's Hospital, Gothenburg, Sweden.

出版信息

Acta Anaesthesiol Scand. 1991 Nov;35(8):745-9. doi: 10.1111/j.1399-6576.1991.tb03383.x.

Abstract

Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were studied in experimental endotoxic shock in dogs. Eight animals were pretreated with a beta-adrenoceptor blocking agent, propranolol (PPL), per os 12 mg/kg once a day for 7 days. Ten animals served as controls. After an intravenous injection of endotoxin, 1 mg/kg, CBF decreased in both groups, with no significant differences between the groups. CMRO2 increased in the control animals by about 18% from the baseline value both 1 and 2 h after the injection of endotoxin. CMRO2 in the PPL-pretreated animals was unchanged after endotoxin. The CMRO2-reactions to endotoxin in control and PPL animals were significantly different after both 1 and 2 h (P less than 0.05). The present results indicate that the increase in CMRO2 following intravenous endotoxin is mediated via beta-adrenoceptors.

摘要

在犬实验性内毒素休克中研究了脑血流量(CBF)和脑氧代谢率(CMRO2)。8只动物口服β-肾上腺素能阻滞剂普萘洛尔(PPL),剂量为12mg/kg,每天1次,共7天。10只动物作为对照。静脉注射1mg/kg内毒素后,两组的CBF均降低,两组之间无显著差异。内毒素注射后1小时和2小时,对照动物的CMRO2较基线值增加约18%。PPL预处理动物在内毒素注射后CMRO2未发生变化。1小时和2小时后,对照动物和PPL处理动物对内毒素的CMRO2反应均有显著差异(P<0.05)。目前的结果表明,静脉注射内毒素后CMRO2的增加是通过β-肾上腺素能受体介导的。

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