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行为应激会改变临界高血压大鼠的冠状动脉血管反应性。

Behavioral stress alters coronary vascular reactivity in borderline hypertensive rats.

作者信息

Fuchs L C, Landas S K, Johnson A K

机构信息

Vascular Biology Center, Medical College of Georgia, Augusta 30912, USA.

出版信息

J Hypertens. 1997 Mar;15(3):301-7. doi: 10.1097/00004872-199715030-00012.

Abstract

BACKGROUND

Behavioral stress has been proposed to contribute to the occurrence of myocardial ischemia. Objective To investigate the effect of chronic exposure to behavioral stress on the function and structure of the coronary artery of borderline hypertensive rats (BHR).

DESIGN

BHR were either exposed to an air-jet stress for 2 h/day for 10 days or kept in their cage for 10 days.

METHODS

After 10 days, hemodynamic measurements in conscious animals were recorded, and their hearts were removed for isolation of a left ventricular coronary artery for functional studies or for fixation by retrograde perfusion for study with scanning electron microscopy. Vascular reactivity was measured in isolated coronary arteries (approximately 250 microm) maintained at an intraluminal diameter of 40 mmHg while the intraluminal diameter was recorded continuously.

RESULTS

The resting mean arterial pressure and heart rate in conscious, unrestrained BHR were not altered significantly by exposure to 10 days of 2 h/day air-jet stress. Coronary artery relaxation in response to the endothelium-dependent vasodilator acetylcholine was impaired in rats exposed to the air-jet stress compared with that in controls. An attenuated response to exogenous nitric oxide in coronary arteries from stressed BHR was confirmed by the finding of a reduced sensitivity to nitroprusside, which releases nitric oxide independently from the endothelium. However, relaxation of coronary arteries in response to isoproterenol, which acts independently from nitric oxide, was not altered. Coronary artery contraction in response to endothelin-1 and phenylephrine was not altered in vessels taken from BHR exposed to behavioral stress compared with that in vessels from control rats. Scanning electron microscopy of the endothelial surface of the septal coronary artery showed no difference between vessels from control and stressed BHR.

CONCLUSION

These results indicate that behavioral stress impairs endothelium-dependent and nitric oxide-mediated coronary relaxation, but does not alter alpha1-adrenoceptor or endothelin-1-mediated contraction. By impairing coronary artery vascular relaxation, chronic exposure to behavioral stress may contribute to myocardial ischemia.

摘要

背景

行为应激被认为与心肌缺血的发生有关。目的:研究长期暴露于行为应激对临界高血压大鼠(BHR)冠状动脉功能和结构的影响。

设计

将BHR分为两组,一组每天接受2小时喷气应激,共10天;另一组在笼中饲养10天。

方法

10天后,记录清醒动物的血流动力学指标,取出心脏,分离左心室冠状动脉用于功能研究,或通过逆行灌注固定用于扫描电子显微镜研究。在管腔内直径维持在40 mmHg的离体冠状动脉(约250微米)中测量血管反应性,同时连续记录管腔内直径。

结果

每天接受2小时、共10天喷气应激的清醒、未束缚BHR的静息平均动脉压和心率无明显改变。与对照组相比,暴露于喷气应激的大鼠对内皮依赖性血管舒张剂乙酰胆碱的冠状动脉舒张功能受损。通过发现对硝普钠(一种独立于内皮释放一氧化氮的物质)的敏感性降低,证实了应激BHR冠状动脉对外源性一氧化氮的反应减弱。然而,对独立于一氧化氮起作用的异丙肾上腺素的冠状动脉舒张反应未改变。与对照大鼠血管相比,暴露于行为应激的BHR血管对内皮素-1和去氧肾上腺素的冠状动脉收缩反应未改变。间隔冠状动脉内皮表面的扫描电子显微镜检查显示,对照和应激BHR的血管之间无差异。

结论

这些结果表明,行为应激损害内皮依赖性和一氧化氮介导的冠状动脉舒张,但不改变α1-肾上腺素能受体或内皮素-1介导的收缩。长期暴露于行为应激通过损害冠状动脉血管舒张,可能导致心肌缺血。

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