By Enalapril, Amlodipine Reversed Hypertensive Rats Cardiovascular Structural Changes In Experimental Research

Left ventricular hypertrophy and aortic hypertrophy caused by hypertension produced many pathological changes.Left ventricular hypertrophy became individual and dangerous factor of the cardiovascular morbidity and mortality.Aortic hypertrophy reduced its conformance,added perivascular resistance,which caused ischia and failure in its target organs. Therefore,it's an important goal to reverse and prevent left ventricular hypertrophy by using all kinds of drugs logically.Now,A number of studies about angiotensin converting enzyme were performed,those about long-acting dihydropyridine calcium antagonist were scarce.This study was to determine the preventive effect of angiotensin-converting enzyme inhibitor and long-acting dihydropyridine calcium antagonist on hypertension,left ventricular and aortic hypertrophy in pressure overload hypertensive rats and the relative importance of cardiomyocyte apoptosis and myocardial fibrosis in ventricular hypertrophy.A suprarenal abdominal aortic band was placed in 60 adult male Wistar rats.Three groups of aortic-banded rats were treated via stomach perfusion with enalapril or ami adipine or combination of both agents. Sham-operated and untreated aortic-banded rats served as controls. Systolic pressure was measured before operation and every two weeks after operation through rats tail volume measure when they were waking and calm.After six weeks,heart and thoracic aorta weredeparted.Left ventricular mass index(LVMI),collagen content in left ventricle,collagen volume fraction(CVF),perivascular circuferential area (PVCA),cardiomyocyte apoptosis index(APOI)and aortic media/lumen ratio were determined by using histomorphological and histochemical methods at six weeks after operation.Firstly,in this study we found that in untreated operated hypertensive group rat hearts got larger and larger,left ventricle became concentric hypertrophy envidently after six weeks,blood pressure,LVMI and cardiac collagen content were higher apparently. Given drugs,cardiac hypertrophy was improved distinctly.Enalapril and amlodipine reduced pressure,LVMI and collagen content efficiently.There was no difference between enalapril and amlodipine treated group.However,the effect in combined group was higher than that in individually used group.Secondly,there were a large number of apoptosis cell and myocardial fibrosis in untreated operated group. Enalapril and amladipine reduced APOI and PVCA,prevented myocardial fibrosis significantly. Their effect was comparable individually.The effect of combination of both drugs was higher.Thirdly.through statistical analysis,we found that LVMI was related with systolic pressure,which meant systolic pressure was very important in left ventricular hypertrophy.At the same time ,APOI was related with CVF ,which hint that myocardial apoptosis and fibrosis were dependent .In the first ,enalapril and amlodipine could inhibit cardiomyocyte apoptosis ,prenent myocardial fibrosis andreverse hypertensive cardiovascular hypertrophy.The effect of combination of both agents was higher. In the second ,there were myocardial apoptosis,perivascular fibrosis and apoptosis in compensatory hypertrophy heart caused by pressure overloading during cardiac remodeling.In the third,we could inhibit left ventricular hypertrophy,cardiomyocyte apoptosis and fibrosis as we reduced blood pressure.