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运动犬心肌功能的α-肾上腺素能调节:突触前α1和α2肾上腺素能受体的证据

Alpha-adrenergic regulation of myocardial performance in the exercising dog: evidence for both presynaptic alpha 1- and alpha 2-adrenoceptors.

作者信息

Guth B D, Thaulow E, Heusch G, Seitelberger R, Ross J

机构信息

Seaweed Canyon Laboratory, Department of Medicine, University of California, La Jolla.

出版信息

Basic Res Cardiol. 1990;85 Suppl 1:131-41. doi: 10.1007/978-3-662-11038-6_11.

Abstract

New evidence supporting both presynaptic alpha 1- and alpha 2-adrenoceptors playing a role in the regulation of myocardial contractile performance in the exercising dog is reviewed. Studies utilized chronically instrumented dogs having sonomicrometers for the measurement of regional wall thickening and transducers for the measurement of left ventricular and systemic hemodynamics. During steady state exercise, either the selective alpha 1-adrenoceptor blocker prazosin (80 micrograms/kg) or the selective alpha 2-adrenoceptor blocker idazoxan (80 micrograms/kg) was infused into the left atrium while exercise continued. Immediately following the administration of either alpha-adrenoceptor blocking agent, there were substantial increases in heart rate, left ventricular dP/dt and regional contractile function as assessed using sonomicrometers, and norepinephrine release by the myocardium increased substantially. beta-adrenergic blockade prevented the heart rate and contractile effects of either alpha 1- or alpha 2-adrenoceptor blocker whereas norepinephrine release was further enhanced. These effects could not be attributed to baroreceptor unloading. In dogs studied under resting conditions with norepinephrine infusion to produce an increase in dP/dt similar to that observed during treadmill exercise, no sympathetic augmentation was observed following either alpha-blocker. Together, these studies provide evidence that both alpha 1- and alpha 2-adrenoceptors participate in the modulation of sympathetic neuronal norepinephrine release in the canine myocardium.

摘要

本文综述了新的证据,支持突触前α1和α2肾上腺素能受体在运动犬心肌收缩性能调节中发挥作用。研究使用了长期植入仪器的犬,这些犬带有用于测量局部心肌增厚的超声微测仪和用于测量左心室及全身血流动力学的传感器。在稳态运动期间,在运动持续的同时,将选择性α1肾上腺素能受体阻滞剂哌唑嗪(80微克/千克)或选择性α2肾上腺素能受体阻滞剂咪唑克生(80微克/千克)注入左心房。在给予任一α肾上腺素能受体阻滞剂后,心率、左心室dP/dt以及使用超声微测仪评估的局部收缩功能均大幅增加,心肌去甲肾上腺素释放也显著增加。β肾上腺素能阻滞可防止α1或α2肾上腺素能受体阻滞剂的心率和收缩效应,而去甲肾上腺素释放则进一步增强。这些效应不能归因于压力感受器卸载。在静息状态下用去甲肾上腺素输注使dP/dt增加至与跑步机运动时相似水平的犬中,给予任一α阻滞剂后均未观察到交感神经增强。总之,这些研究提供了证据,表明α1和α2肾上腺素能受体均参与犬心肌中交感神经元去甲肾上腺素释放的调节。

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