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降温是大鼠深部血管的一种强效血管舒张剂。

Cooling is a potent vasodilator of deep vessels in the rat.

作者信息

Mustafa S, Thulesius O

机构信息

Department of Pharmacology and Toxicology, Faculty of Medicine, Kuwait University, Safat.

出版信息

Can J Physiol Pharmacol. 2001 Nov;79(11):899-904.

Abstract

The objectives of this study were to determine the effect of cooling on smooth muscle tone of the pulmonary artery and aorta and to clarify the basic mechanism of these responses. We recorded isometric tension in smooth muscle strips of rat pulmonary artery and aorta in organ baths during stepwise cooling. Cooling responses were tested before and after the addition of various standard agents that interfere with known neurogenic (autonomic blockers, tetrodotoxin) and myogenic mechanisms (calcium channel blockers) of relaxation. We also examined the hypothesis of the presence of a cooling-released substance. Stepwise cooling (37degrees C to 4 degrees C) of aortic smooth muscle induced reproducible graded relaxations that were inversely proportional to temperature. Cooling-induced relaxation was not dependent on a neural mechanism nor the release of neurotransmitters or a cooling-released substance such as NO or CO. Cooling of pulmonary arterial and aortic smooth muscle preparations induced a graded myogenic relaxation inversely proportional to the cooling temperature. The mechanism is not dependent on local nervous or known mediators but related to a direct physico-chemical effect of cooling.

摘要

本研究的目的是确定冷却对肺动脉和主动脉平滑肌张力的影响,并阐明这些反应的基本机制。我们在器官浴中逐步冷却过程中记录大鼠肺动脉和主动脉平滑肌条的等长张力。在添加各种干扰已知神经源性(自主阻滞剂、河豚毒素)和肌源性舒张机制(钙通道阻滞剂)的标准试剂之前和之后测试冷却反应。我们还检验了存在冷却释放物质的假设。主动脉平滑肌的逐步冷却(37℃至4℃)诱导了可重复的分级舒张,其与温度成反比。冷却诱导的舒张不依赖于神经机制,也不依赖于神经递质或冷却释放物质(如NO或CO)的释放。肺动脉和主动脉平滑肌制剂的冷却诱导了与冷却温度成反比的分级肌源性舒张。其机制不依赖于局部神经或已知介质,而是与冷却的直接物理化学效应有关。

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