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急性冠状动脉闭塞及随后的β2和α1肾上腺素能阻断时心脏的局部灌注

Regional perfusion in hearts with acute coronary artery occlusion and subsequent beta 2- and alpha 1-adrenergic blockade.

作者信息

Kvitting P, Westby J, Birkeland S, Lekven J, Grong K

机构信息

Department of Surgery, University of Bergen, Haukeland Hospital, Norway.

出版信息

Clin Physiol. 1990 Mar;10(2):155-70. doi: 10.1111/j.1475-097x.1990.tb00250.x.

DOI:10.1111/j.1475-097x.1990.tb00250.x
PMID:1969337
Abstract

Blockade of cardiac adrenoceptor subtypes, coronary or myocardial, might elicit compensatory interaction from remaining unblocked subtypes. An attempt to explore this interplay was made by studying regional myocardial blood flow alterations associated with beta 2-adrenergic blockade followed by alpha 1-adrenergic blockade in anaesthetized cats with acute coronary occlusion. In order to maintain constant needs for perfusion, atrial pacing was established and the aortic blood pressure was kept constant. In myocardium remote from the ischaemic region, beta 2-adrenergic blockade produced higher endocardial blood flow whereas no flow changes were observed close to the ischaemic region. With subsequent alpha 1-adrenergic blockade, blood flow increased endocardially in non-ischaemic regions, but remained unchanged in epicardial tissue. Control experiments without coronary ligation revealed no increase in left ventricular oxygen consumption during the experiments and support the theory that the observed blood flow increase in the coronary ligation group, following drug interventions, was not caused by increased cardiac work. This study indicates that combined beta 2- and alpha 1-adrenergic blockade alters the balance between receptor subtypes. Unopposed beta 1-mediated vasodilation is the most likely candidate to explain why endocardial flow was increased.

摘要

阻断心脏肾上腺素能受体亚型,无论是冠状动脉还是心肌的,都可能引发其余未被阻断的亚型的代偿性相互作用。通过研究在急性冠状动脉闭塞的麻醉猫中,先进行β2肾上腺素能阻断,随后进行α1肾上腺素能阻断时相关的区域心肌血流改变,来尝试探究这种相互作用。为了维持恒定的灌注需求,建立了心房起搏并保持主动脉血压恒定。在远离缺血区域的心肌中,β2肾上腺素能阻断使心内膜血流增加,而在靠近缺血区域未观察到血流变化。随后进行α1肾上腺素能阻断时,非缺血区域的心内膜血流增加,但心外膜组织血流保持不变。未进行冠状动脉结扎的对照实验显示实验期间左心室氧消耗没有增加,支持了以下理论:在药物干预后,冠状动脉结扎组中观察到的血流增加并非由心脏做功增加引起。这项研究表明,联合β2和α1肾上腺素能阻断会改变受体亚型之间的平衡。未受对抗的β1介导的血管舒张最有可能解释心内膜血流增加的原因。

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