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肾性高血压犬的腺苷与冠状动脉血流的代谢调节

Adenosine and metabolic regulation of coronary blood flow in dogs with renal hypertension.

作者信息

Ely S W, Sun C W, Knabb R M, Gidday J M, Rubio R, Berne R M

出版信息

Hypertension. 1983 Nov-Dec;5(6):943-50. doi: 10.1161/01.hyp.5.6.943.

DOI:10.1161/01.hyp.5.6.943
PMID:6228529
Abstract

It has been demonstrated that resting coronary vascular resistance is elevated with chronic hypertension and concomitant cardiac hypertrophy. The present study employed a model of 6-week, one-kidney, one wrapped Page hypertension to determine if the ability of the heart to match an increase in oxygen demand with an increase in oxygen supply (coronary blood flow) is impaired, and to determine if these vasoregulatory abnormalities are attributable to inadequate adenosine release. Studies were performed in a pentobarbital anesthetized, open-chest canine preparation using a pericardial infusate method to determine adenosine release. Results showed that dobutamine (a beta-receptor agonist) induced increases in myocardial oxygen consumption (MVO2) over a physiological range (8-30 ml O2 X min-1 X 100 g-1) that were accompanied by an increase in coronary blood flow (CBF) with no change in oxygen extraction. The relationship between MVO2 and CBF was not different between the normotensive (NTC) and hypertensive (RHT) animals. Pericardial infusate adenosine (PI ADO) concentrations were not different for the same MVO2 and CBF, and the relationships for MVO2 vs PI ADO as well as PI ADO vs CBF were unaltered by hypertension. However, the relationship between PI ADO and coronary vascular resistance (CVR) was altered in the RHT group such that a given PI ADO concentration was associated with a significantly higher CVR. These data suggest that, over the range of MVO2 studied, there are no limitations in metabolic regulation of the coronary circulation of RHT animals, and that the higher CVR encountered in the RHT group is not the result of a reduced release of the endogenous vasodilator, adenosine.

摘要

已有研究表明,慢性高血压及伴随的心脏肥大可使静息冠状血管阻力升高。本研究采用为期6周的单肾、单包被佩奇高血压模型,以确定心脏使氧需求增加与氧供应增加(冠状血流量)相匹配的能力是否受损,并确定这些血管调节异常是否归因于腺苷释放不足。研究在戊巴比妥麻醉、开胸犬模型上进行,采用心包灌注法测定腺苷释放。结果显示,多巴酚丁胺(一种β受体激动剂)在生理范围内(8 - 30 ml O2·min-1·100 g-1)诱导心肌耗氧量(MVO2)增加,同时冠状血流量(CBF)增加,而氧摄取无变化。正常血压(NTC)和高血压(RHT)动物的MVO2与CBF之间的关系无差异。相同MVO2和CBF时,心包灌注液腺苷(PI ADO)浓度无差异,高血压也未改变MVO2与PI ADO以及PI ADO与CBF之间的关系。然而,RHT组中PI ADO与冠状血管阻力(CVR)之间的关系发生了改变,即给定的PI ADO浓度与显著更高的CVR相关。这些数据表明,在所研究的MVO2范围内,RHT动物冠状循环的代谢调节没有限制,且RHT组中遇到的较高CVR并非内源性血管舒张剂腺苷释放减少的结果。

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