Effects of benazepril on cardiac function, free oxygen radicals, sarcoplasmic reticulum Ca~(2+)- ATPase following cardiac ischemia- reperfusion in spontaneously hypertensive rats
- VernacularTitle:苯那普利对自发性高血压大鼠心肌缺血-再灌注心功能、氧自由基和肌浆网Ca~(2+)-ATP酶的影响
- Author:
Yesong WANG
;
Hong MA
;
Jianwen CHEN
;
Yuan HU
;
Xiujian LAN
;
Fanhua QIU
- Publication Type:Journal Article
- Keywords:
Benazepril;
Ischemia-reperfusion;
Cardiac function;
Free oxygen radicals;
Ca~(2+)-ATPase
- From:
Chinese Journal of Pathophysiology
1986;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effects of angiotensin converting enzyme inhibitor (ACEI), benazepril(B), on cardiac function, free oxygen radicals, sarcoplasmic reticulum(SR) Ca~(2+)-ATPase following ischemia-reper-fusion in sportaneously hypertensive rats (SHRs). METHODS: Thirty 10-week-old female SHRs were randomly assigned into two groups: group SHR was control; The animal in group SHR+B was given with 10 mg/kg of benazepril perday. Another 15 Wistar rats with the same age and sex were normal control (group Wistar). After 12 weeks of pretreatment, all rats in each group were subjected to 30 min of left anterior descending coronary artery occlusion and 30 min of reperfusion. Hemodynamic parameters, left heart-to-body weight ratio(LVW/BW), myocardial malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity, and SR Ca~(2+)-ATPase activity were measured. RESULTS: Compared to group Wistar, the rats in group SHR had higher blood pressure, LVW/BW and myocardial MDA concentration, more serious left cardiac function injury and lower myocardial SOD activity and SR Ca~(2+)-ATPase activity; group SHR+B had lower myocardial MDA concentration, higher myocardial SOD activity, but no difference in blood pressure, LVW/BW, the degree of left cardiac function injury and myocardial SR Ca~(2+)-ATPase activity. CONCLUSION: Benazepril can attenuate ischemia-reperfusion-induced cardiac function injury by regression of left ventricular hypertrophy (LVH), improving SR Ca~(2+)-ATPase activity and decreasing oxygen free radicals injury in SHRs.
