HYPOXIA RELEASES A VASOCONSTRICTOR SUBSTANCE FROM THE CANINE VASCULAR ENDOTHELIUM

HYPOXIA RELEASES A VASOCONSTRICTOR SUBSTANCE FROM THE CANINE VASCULAR ENDOTHELIUM
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DOI:
10.1113/jphysiol.1985.sp015728
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发表时间:
1985-01-01
影响因子:
5.5
通讯作者:
VANHOUTTE, PM
VANHOUTTE, PM
中科院分区:
医学1区
文献类型:
--
作者:
RUBANYI, GM;VANHOUTTE, PM

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实验旨在确定内皮细胞在缺氧易化离体冠状动脉收缩反应中的作用。犬冠状动脉环和条,有或无内皮,悬挂在改良Krebs-Ringer碳酸氢盐溶液中进行等长张力记录。为了确定血管活性物质从内皮细胞的释放,将不含内皮的条带与含内皮的条带分层。在具有内皮的环和分层制剂中,缺氧(95%N2 - 5%CO2)增强了对前列腺素F2 α的收缩反应。缺氧(10或5%O2)引起的收缩在消炎痛的存在。去除内皮后,缺氧易化和缺氧收缩均消失。环氧合酶、脂氧合酶或磷脂酶A2或肾上腺素能、肾上腺素能和组胺能受体的抑制剂不能阻止对缺氧的反应。同样,内皮衍生因子的抑制剂(奎纳克林,菲尼酮和亚甲蓝)不影响缺氧易化。缺氧、缺氧可引起无内皮冠状动脉与有内皮的股动、静脉重叠后收缩。在股动脉中观察到了厌食促进作用,但在有内皮的股静脉中没有观察到。这些实验表明,低氧和缺氧引起内皮细胞释放可扩散的血管收缩物质。不同解剖来源的平滑肌对易化介质的敏感性不同。
Experiments were designed to determine the role of the endothelium in the facilitation by anoxia of contractile responses of isolated coronary arteries. Rings and strips of canine coronary arteries, with or without endothelium, were suspended for isometric tension recording in modified Krebs-Ringer bicarbonate solution. To determine the release of a vasoactive substance(s) from the endothelial cells, strips without endothelium were layered with strips containing endothelium. In rings and in layered preparations with endothelium, anoxia (95% N2-5% CO2) augmented contractile responses to prostaglandin F2.alpha.. Hypoxia (10 or 5% O2) caused contractions in the presence of indomethacin. Removal of the endothelium abolished the anoxic facilitation and the hypoxic contractions. Inhibitors of cyclo-oxygenase, lipoxygenase or phospholipase A2 or of adrenergic, serotonergic and histaminergic receptors did not prevent the response to anoxia. Likewise, inhibitors of the endothelium-derived factor(s) (quinacrine, phenidone and methylene blue) did not affect the anoxic facilitation. Hypoxia and anoxia caused contraction of coronary arteries without endothelium when layered with femoral arteries and veins with endothelium. Anoxic facilitation was observed in femoral arteries, but not in femoral veins, with endothelium. These experiments indicate that hypoxia and anoxia cause the release of a diffusible vasoconstrictor substance(s) from endothelial cells. The sensitivity of smooth muscle of different anatomical origin to the facilitatory mediator(s) varies.