Role of adenosine in norepinephrine-induced coronary vasodilation.
Role of adenosine in norepinephrine-induced coronary vasodilation.
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腺苷在去甲肾上腺素诱导的冠状血管舒张中的作用。
DOI：
10.1152/ajpheart.1997.273.2.h557
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Feigl,EO
中科院分区：
文献类型：
--
作者：
VanBibber,R;Stepp,DW;Kroll,K;Feigl,EO
腺苷被认为是冠状动脉血流增加与心肌代谢增加的生理递质耦合。本实验的目的是评价腺苷在去甲肾上腺素引起的冠状动脉充血中的作用。在11只麻醉闭胸犬制剂中，左冠状动脉主动脉插管并灌注100 mmHg的血液。测量冠状动脉血流量和心肌耗氧量，并使用分布式模型从动脉和冠状静脉测量中估计间质腺苷浓度。用8-苯基茶碱（8-PT）阻断腺苷受体，使腺苷剂量-反应曲线位移12倍。在冠状动脉内灌注去甲肾上腺素时，冠状动脉血流量和心肌耗氧量在8-PT前后相似地增加，表明腺苷受体阻断缺乏作用。8-PT前，估计间质腺苷升高至血管活性浓度（220 nM）；然而，与冠状动脉血流的时间相关性较差。8-PT后，发现估计间质腺苷也有类似的增加，表明腺苷浓度没有增加以克服腺苷受体阻断。因此，腺苷不能对腺苷受体阻断后冠状动脉血流量的增加负责，因此，去甲肾上腺素诱导的充血不需要腺苷。
Adenosine has been postulated to be the physiological transmitter coupling increases in coronary blood flow to increases in myocardial metabolism. The purpose of this experiment was to evaluate the role of adenosine in the coronary hyperemia due to norepinephrine. In 11 anesthetized, closed-chest canine preparations, the left main coronary artery was cannulated and perfused with blood at 100 mmHg. Coronary blood flow and myocardial oxygen consumption were measured, and interstitial adenosine concentration was estimated from arterial and coronary venous measurements using a distributed model. Adenosine receptor blockade with 8-phenyltheophylline (8-PT) was used to shift the adenosine dose-response curve 12-fold. During intracoronary norepinephrine infusion, coronary blood flow and myocardial oxygen consumption increased similarly before and after 8-PT, demonstrating a lack of an effect from the adenosine receptor blockade. Before 8-PT, estimated interstitial adenosine increased to a vasoactive concentration (220 nM); however, the temporal correlation with coronary blood flow was poor. After 8-PT, a similar increase in estimated interstitial adenosine was found, demonstrating that there was no augmentation in adenosine concentration to overcome the adenosine receptor blockade. Thus adenosine could not be responsible for the increase in coronary blood flow after adenosine receptor blockade and therefore is not required for norepinephrine-induced hyperemia.