Department of Physiology II, Kanazawa Medical University, Uchinada, Japan; and.
Am J Physiol Regul Integr Comp Physiol. 2013 Oct 15;305(8):R900-7. doi: 10.1152/ajpregu.00120.2013. Epub 2013 Aug 15.
Anaphylactic shock is sometimes life-threatening, and it is accompanied by hepatic venoconstriction in animals, which, in part, accounts for anaphylactic hypotension. Roles of norepinephrine and α-adrenoceptor in anaphylaxis-induced hypotension and portal hypertension were investigated in anesthetized ovalbumin-sensitized Sprague-Dawley rats. The sensitized rats were randomly allocated to the following pretreatment groups (n = 6/group): 1) control (nonpretreatment), 2) α1-adrenoceptor antagonist prazosin, 3) nonselective α-adrenoceptor antagonist phentolamine, 4) 6-hydroxydopamine-induced chemical sympathectomy, and 5) surgical hepatic sympathectomy. Anaphylactic shock was induced by an intravenous injection of the antigen. The systemic arterial pressure (SAP), central venous pressure (CVP), portal venous pressure (PVP), and portal venous blood flow (PBF) were measured, and splanchnic [Rspl: (SAP-PVP)/PBF] and portal venous [Rpv: (PVP-CVP)/PBF] resistances were determined. Separately, we measured efferent hepatic sympathetic nerve activity during anaphylaxis. In the control group, SAP markedly decreased, followed by a gradual recovery toward baseline. PVP and Rpv increased 3.2- and 23.3-fold, respectively, after antigen. Rspl decreased immediately, but only transiently, after antigen, and then increased 1.5-fold later than 10 min. The α-adrenoceptor antagonist pretreatment or chemical sympathectomy inhibited the late increase in Rspl and the SAP recovery. Pretreatment with α-adrenoceptor antagonists, or either chemical or surgical hepatic sympathectomy, did not affect the antigen-induced increase in Rpv. Hepatic sympathetic nerve activity did not significantly change after antigen. In conclusion, α-adrenoceptor antagonists and chemical sympathectomy exacerbate anaphylaxis-induced hypotension, but not portal hypertension, in anesthetized rats. Hepatic sympathetic nerves are not involved in anaphylactic portal hypertension.
过敏性休克有时是致命的，它伴随着动物的肝静脉收缩，这在一定程度上导致了过敏性低血压。本研究旨在探讨去甲肾上腺素和α-肾上腺素受体在卵清蛋白致敏 Sprague-Dawley 大鼠过敏性休克低血压和门静脉高压中的作用。致敏大鼠随机分为以下预处理组（每组 n = 6）：1）对照组（未预处理）、2）α1-肾上腺素受体拮抗剂哌唑嗪、3）非选择性α-肾上腺素受体拮抗剂酚妥拉明、4）6-羟多巴胺诱导的化学性交感神经切除术和 5）手术性肝交感神经切除术。通过静脉注射抗原诱导过敏性休克。测量系统动脉压（SAP）、中心静脉压（CVP）、门静脉压（PVP）和门静脉血流量（PBF），并测定内脏[Rspl：（SAP-PVP）/PBF]和门静脉[Rpv：（PVP-CVP）/PBF]阻力。此外，我们在过敏性休克期间测量了传出性肝交感神经活动。在对照组中，SAP 明显下降，随后逐渐恢复到基线水平。抗原后 PVP 和 Rpv 分别增加了 3.2 倍和 23.3 倍。Rspl 在抗原后立即下降，但仅短暂下降，然后在 10 分钟后增加 1.5 倍。α-肾上腺素受体拮抗剂预处理或化学性交感神经切除术抑制了 Rspl 的晚期增加和 SAP 的恢复。α-肾上腺素受体拮抗剂预处理或肝交感神经切除术均不影响抗原诱导的 Rpv 增加。抗原后肝交感神经活动无明显变化。综上所述，α-肾上腺素受体拮抗剂和化学性交感神经切除术加重了麻醉大鼠过敏性休克引起的低血压，但不加重门静脉高压。肝交感神经不参与过敏性门静脉高压。
