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短吻鳄(密西西比鳄)肺内动脉的低氧诱导血管收缩:内皮素-1的作用?

Hypoxia-induced vasoconstriction in alligator (Alligator mississippiensis) intrapulmonary arteries: a role for endothelin-1?

作者信息

Skovgaard Nini, Zibrandtsen Helle, Laursen Britt Elmedal, Simonsen Ulf, Wang Tobias

机构信息

Zoophysiology, Department of Biological Sciences, University of Aarhus, Building 1131, 8000 Aarhus C, Denmark.

出版信息

J Exp Biol. 2008 May;211(Pt 10):1565-70. doi: 10.1242/jeb.014662.

DOI:10.1242/jeb.014662
PMID:18456883
Abstract

Hypoxic pulmonary vasoconstriction (HPV) is an adaptive response that diverts pulmonary blood flow from poorly ventilated and hypoxic areas of the lung to better ventilated parts, matching blood perfusion to ventilation. HPV is an ancient and highly conserved response expressed in the respiratory organs of all vertebrates. However, the underlying mechanism and the role of the endothelium remain elusive. Isolated intrapulmonary arteries (internal diameter <346 microm) from the American alligator Alligator mississippiensis were mounted in microvascular myographs for isometric tension recording. Resting vessels and vessels contracted with either serotonin (5-HT) or endothelin-1 (ET-1) were exposed to sustained (45 min) hypoxia (PO2<5 mmHg). In ET-1-contracted vessels, hypoxia induced a monophasic, sustained and fully reversible constriction, which was independent of the endothelium. In relaxed or in 5-HT-contracted vessels, hypoxia did not cause constriction. The effects of ET-1, ET(A) and ET(B) as well as the general ET-receptor antagonist were studied. ET-1 caused a contraction of the pulmonary arteries through stimulation of ET(A)-receptors. ET(A) and ET(B) immunoreactive staining revealed the location of both receptors in the smooth muscle layer and of ET(B) receptors in the endothelium. In conclusion, because precontraction with serotonin did not facilitate HPV, the required precontraction in alligators seems specific to ET-1, which implies that ET-1 plays an important permissive role for the HPV response in alligators.

摘要

缺氧性肺血管收缩(HPV)是一种适应性反应,可将肺血流从肺通气不良和缺氧的区域转移至通气较好的部位,使血液灌注与通气相匹配。HPV是一种古老且高度保守的反应,在所有脊椎动物的呼吸器官中均有表达。然而,其潜在机制以及内皮的作用仍不明确。将来自美国短吻鳄密西西比鳄的离体肺内动脉(内径<346微米)安装在微血管肌动描记器中以记录等长张力。将静息血管以及用5-羟色胺(5-HT)或内皮素-1(ET-1)收缩后的血管暴露于持续(45分钟)缺氧(PO2<5 mmHg)环境中。在ET-1收缩的血管中,缺氧诱导单相、持续且完全可逆的收缩,这与内皮无关。在松弛或5-HT收缩的血管中,缺氧未引起收缩。研究了ET-1、ET(A)和ET(B)以及通用ET受体拮抗剂的作用。ET-1通过刺激ET(A)受体引起肺动脉收缩。ET(A)和ET(B)免疫反应性染色揭示了两种受体在平滑肌层中的位置以及ET(B)受体在内皮中的位置。总之,由于用5-羟色胺预收缩并未促进HPV,短吻鳄中所需的预收缩似乎对ET-1具有特异性,这意味着ET-1在短吻鳄的HPV反应中起重要的允许作用。

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