Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice
Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice
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DOI：
10.1152/ajpregu.00904.2006
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发表时间：
2007-11-01
影响因子：
2.8
通讯作者：
Kurata, Yasutaka
中科院分区：
文献类型：
--
作者：
Liu, Wei;Takano, Hiromichi;Kurata, Yasutaka
采用BALB/c小鼠体内和离体灌注肝制剂，探讨肝脏和内脏血管床在过敏性低血压中的作用。完整致敏小鼠静脉注射卵清蛋白抗原可使全身动脉压（P-sa）从92 +/- 2 (SE) mmHg降至39 +/- 3 (SE) mmHg，但门静脉压（P-pv）仅在抗原后3.5 min从6.4 +/- 0.1 cmH(2)O略微升高至9.9 +/- 0.5 cmH(2)O的峰值。腹腔和肠系膜动脉结扎消除内脏血管床，并联合全肝切除术，减轻过敏性低血压。单独结扎这些动脉，但不切除部分肝（70%），同样可以减轻过敏性低血压。相比之下，以恒流量门静脉灌注的离体致敏小鼠肝脏没有出现过敏性静脉收缩，而是对过敏相关的血小板活化因子的反应出现了实质性的收缩，这表明小鼠体内的静脉收缩可能是由肝外组织释放的介质诱导的。这些结果表明，内脏血管床参与了BALB/c小鼠过敏性低血压。它们可能作为化学介质的来源，引起过敏反应引起的门静脉高压，引起内脏充血，导致循环血容量减少，从而导致全身动脉低血压。小鼠肝过敏性静脉收缩可能由肝外因素引起，而不是由肝内过敏反应引起。
Using in vivo and isolated perfused liver preparations of BALB/c mice, we determined the roles of the liver and splanchnic vascular bed in anaphylactic hypotension. Intravenous injection of ovalbumin antigen into intact-sensitized mice decreased systemic arterial pressure (P-sa) from 92 +/- 2 to 39 +/- 3 ( SE) mmHg but only slightly increased portal venous pressure (P-pv) from 6.4 +/- 0.1 cmH(2)O to the peak of 9.9 +/- 0.5 cmH(2)O at 3.5 min after antigen. Elimination of the splanchnic vascular beds by ligation of the celiac and mesenteric arteries, combined with total hepatectomy, attenuated anaphylactic hypotension. Ligation of these arteries alone, but not partial hepatectomy (70%), similarly attenuated anaphylactic hypotension. In contrast, isolated sensitized mouse liver perfused portally at constant flow did not show anaphylactic venoconstriction but, rather, substantial constriction in response to the anaphylaxis-associated platelet-activating factor, indicating that venoconstriction in mice in vivo may be induced by mediators released from extrahepatic tissues. These results suggest that splanchnic vascular beds are involved in BALB/c mouse anaphylactic hypotension. They presumably act as sources of chemical mediators to cause the anaphylaxis-induced portal hypertension, which induced splanchnic congestion, resulting in a decrease in circulating blood volume and, thus, systemic arterial hypotension. Mouse hepatic anaphylactic venoconstriction may be induced by factors outside the liver, but not by anaphylactic reaction within the liver.