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慢性身心应激诱导对雄性大鼠离体心脏心肌缺血/再灌注损伤的评估:交感神经系统的作用

Evaluation of Chronic Physical and Psychological Stress Induction on Cardiac Ischemia / Reperfusion Injuries in Isolated Male Rat Heart: The Role of Sympathetic Nervous System.

作者信息

Rakhshan Kamran, Imani Alireza, Faghihi Mahdieh, Nabavizadeh Fatemeh, Golnazari Masoumeh, Karimian SeyedMorteza

机构信息

Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Department of Physiology, Occupational Sleep Research Center Tehran, Tehran, Iran.

出版信息

Acta Med Iran. 2015 Aug;53(8):482-90.

Abstract

Exposure to stress leads to physiological changes called "stress response" which are the result of the changes in the adrenomedullary hormone system, hypothalamus-pituitary-adrenal (HPA) and sympathetic nervous system (SNS) activity. In the present study, the effects of chronic physical and psychological stress and also the role of sympathetic system effects in stress on ischemia/reperfusion (I/R) injuries have been studied in isolated rat heart. Rat heart was isolated and subjected to 30 min regional ischemia and 120 min reperfusion. The daily stress was induced for one week prior to I/R induction. Sympathectomy was done chemically by injection of hydroxyl-dopamine prior to stress induction. There were no significant changes in heart rate and Coronary Flow between groups. Left ventricular developed pressure (LVDP) and rate product pressure (RPP) in both physical and psychological stress groups decreased significantly compared to those in control group (P<0.05), but there was no significant difference between physical and psychological stress groups. Infarct size significantly increased in both physical and psychological stress groups and control group(P<0.05. Sympathectomy before induction of stress led to the elimination of the deleterious effects of stress as compared with stress groups (P<0.05). These results show that induction of chronic physical and psychological stress prior to ischemia/reperfusion causes enhancement of myocardial injuries and it seems that increased sympathetic activity in response to stress is responsible for these adverse effects of stress on ischemic/reperfused heart.

摘要

暴露于应激状态会导致称为“应激反应”的生理变化,这是肾上腺髓质激素系统、下丘脑 - 垂体 - 肾上腺(HPA)和交感神经系统(SNS)活动变化的结果。在本研究中,在离体大鼠心脏中研究了慢性身体和心理应激的影响以及交感神经系统效应在应激对缺血/再灌注(I/R)损伤中的作用。分离大鼠心脏,使其经历30分钟的局部缺血和120分钟的再灌注。在诱导I/R前一周诱导每日应激。在应激诱导前通过注射羟基多巴胺进行化学性交感神经切除术。各组之间心率和冠状动脉血流量无显著变化。与对照组相比,身体和心理应激组的左心室舒张末压(LVDP)和心率与收缩压乘积(RPP)均显著降低(P<0.05),但身体和心理应激组之间无显著差异。身体和心理应激组以及对照组的梗死面积均显著增加(P<0.05)。与应激组相比,应激诱导前进行交感神经切除术可消除应激的有害影响(P<0.05)。这些结果表明,在缺血/再灌注前诱导慢性身体和心理应激会导致心肌损伤加重,并且似乎应激反应中交感神经活动增加是应激对缺血/再灌注心脏产生这些不利影响的原因。

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