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肝静脉收缩与大鼠过敏性低血压有关。

Hepatic venoconstriction is involved in anaphylactic hypotension in rats.

作者信息

Shibamoto Toshishige, Cui Sen, Ruan Zonghai, Liu Wei, Takano Hiromichi, Kurata Yasutaka

机构信息

Department of Physiology, Kanazawa Medical University, Uchinada Ishikawa 920-0293, Japan.

出版信息

Am J Physiol Heart Circ Physiol. 2005 Oct;289(4):H1436-41. doi: 10.1152/ajpheart.00368.2005. Epub 2005 May 27.

DOI:10.1152/ajpheart.00368.2005
PMID:15923315
Abstract

We determined the roles of liver and splanchnic vascular bed in anaphylactic hypotension in anesthetized rats and the effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused rat livers. In anesthetized rats sensitized with ovalbumin (1 mg), an intravenous injection of 0.6 mg ovalbumin caused not only a decrease in systemic arterial pressure from 120 +/- 9 to 43 +/- 10 mmHg but also an increase in portal venous pressure that persisted for 20 min after the antigen injection (the portal hypertension phase). The elimination of the splanchnic vascular beds, by the occlusions of the celiac and mesenteric arteries, combined with total hepatectomy attenuated anaphylactic hypotension during the portal hypertension phase. For the isolated perfused rat liver experiment, the livers derived from sensitized rats were hemoperfused via the portal vein at a constant flow. Using the double-occlusion technique to estimate the hepatic sinusoidal pressure, presinusoidal (R(pre)) and postsinusoidal (R(post)) resistances were calculated. An injection of antigen (0.015 mg) caused venoconstriction characterized by an almost selective increase in R(pre) rather than R(post) and liver weight loss. Taken together, these results suggest that liver and splanchnic vascular beds are involved in anaphylactic hypotension presumably because of anaphylactic presinusoidal contraction-induced portal hypertension, which induced splanchnic congestion resulting in a decrease in circulating blood volume and thus systemic arterial hypotension.

摘要

我们确定了肝脏和内脏血管床在麻醉大鼠过敏性低血压中的作用,以及过敏反应对离体灌注大鼠肝脏肝血管阻力和肝脏重量的影响。在用卵清蛋白(1毫克)致敏的麻醉大鼠中,静脉注射0.6毫克卵清蛋白不仅使体动脉压从120±9毫米汞柱降至43±10毫米汞柱,还使门静脉压升高,抗原注射后该压力持续20分钟(门静脉高压期)。通过阻断腹腔动脉和肠系膜动脉消除内脏血管床,并结合全肝切除术,可减轻门静脉高压期的过敏性低血压。对于离体灌注大鼠肝脏实验,将致敏大鼠的肝脏经门静脉以恒定流量进行血液灌注。使用双阻断技术估计肝窦压力,计算窦前(R(pre))和窦后(R(post))阻力。注射抗原(0.015毫克)导致静脉收缩,其特征是R(pre)几乎选择性增加而非R(post),并伴有肝脏重量减轻。综上所述,这些结果表明肝脏和内脏血管床参与了过敏性低血压,推测是由于过敏反应引起的窦前收缩导致门静脉高压,进而引起内脏充血,导致循环血容量减少,从而导致体动脉低血压。

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