Hepatic venoconstriction is involved in anaphylactic hypotension in rats
Hepatic venoconstriction is involved in anaphylactic hypotension in rats
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DOI：
10.1152/ajpheart.00368.2005
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发表时间：
2005-10-01
影响因子：
4.8
通讯作者：
Kurata, Y
中科院分区：
文献类型：
--
作者：
Shibamoto, T;Cui, S;Kurata, Y
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流大鼠肝脏的肝血管阻力和肝脏重量的影响。在用卵清蛋白（1 mg）致敏的麻醉大鼠中，静脉注射0.6 mg卵清蛋白不仅导致全身动脉压从120 +/- 9降至43 +/- 10 mmHg，而且导致门静脉压升高，并在抗原注射后持续20 min（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，结合全肝切除术，减轻了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，通过门静脉以恒定流量对来自致敏大鼠的肝脏进行血液灌流。使用双闭塞技术估计肝窦压力，计算窦前（R-pre）和窦后（R-post）阻力。注射抗原（0.015 mg）引起静脉收缩，其特征在于几乎选择性增加R-前，而不是R-后和肝脏重量减轻。两者合计，这些结果表明，肝脏和内脏血管床参与过敏性低血压，大概是因为过敏性窦前收缩诱导的门静脉高压，引起内脏充血，导致循环血容量减少，从而全身动脉低血压。
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.