PRESERVATION OF LEFT-VENTRICULAR FUNCTION AND CORONARY FLOW BY ANGIOTENSIN I-CONVERTING ENZYME-INHIBITION IN THE HYPERTENSIVE-DIABETIC DAHL RAT

被引：13

作者：

GIVEN, MB ^{[1
]}

LOWE, RF ^{[1
]}

GELVIN, CR ^{[1
]}

SANDER, GE ^{[1
]}

GILES, TD ^{[1
]}

机构：

[1] LOUISIANA STATE UNIV,SCH MED,DEPT MED,CARDIOL SECT,NEW ORLEANS,LA 70112

来源：

AMERICAN JOURNAL OF HYPERTENSION | 1994年 / 7卷 / 10期

关键词：

DIABETES MELLITUS; STREPTOZOTOCIN; CARDIOMYOPATHY DAHL RATS; ANGIOTENSIN I-CONVERTING ENZYME; HYPERTENSION;

D O I：

10.1093/ajh/7.10.919

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

The effect of the angiotensin I-converting enzyme (ACE) inhibitor benazepril (55 mg/kg orally) on the preservation of cardiac performance in diabetic-hypertensive Dahl S rats was investigated. Diabetes mellitus was produced by streptozotocin. Fasting (4-h) blood glucose levels were 279 +/- 50 mg/dL in diabetic Dahl salt-sensitive v 79 +/- 5 mg/dL in nondiabetic Dahl salt-sensitive rats. Cardiac performance was determined at the end of 8 weeks in an isolated perfused working heart apparatus. Peak left ventricular pressure (LVP(max)), left ventricular peak negative dP/dt, and coronary flow were depressed in diabetic Dahl S rats (P less than or equal to .05 v control). These deficits in cardiac function were not observed in diabetic Dahl S rats chronically treated with benazepril. The beneficial effects of benazepril apparently were independent of systolic blood pressure reduction. Although plasma ACE activity was increased in diabetic Dahl S rats, plasma renin activity was reduced. This suggests that the beneficial effects of ACE inhibition may be due to an effect upon the kinin system rather than the renin-angiotensin system. The benazepril-associated preservation of cardiac function in this study suggests that ACE inhibitors may be beneficial in the treatment of diabetic heart disease.

引用

页码：919 / 925

页数：7

共 34 条

[1]

Kannel W.B., Hjortland M., Castelli W.P., Role of diabetes in congestive heart failure: The Framingham study, Am J Cardiol, 34, pp. 29-34, (1974)

[2]

Rubier S., Dlugash J., Yuceoglu Y.Z., Et al., New type of cardiomyopathy associated with diabetic glomerulosclerosis, Am J Cardiol, 30, pp. 595-602, (1972)

[3]

Ahmed S.S., Jaferi G.A., Narang R.M., Et al., Preclinical abnormalities of left ventricular function in diabetes mellitus, Am Heart J, 89, pp. 153-158, (1975)

[4]

Regan T.J., Lyons M.M., Ahmed S.S., Et al., Evidence for cardiomyopathy in familial diabetes mellitus, J Clin Invest, 60, pp. 885-899, (1977)

[5]

Regan T.I., Ettinger P.O., Kahn M.I., Et al., Altered myocardial function and metabolism in chronic diabetes mellitus without ischemia in dogs, Circ Res, 35, pp. 222-237, (1974)

[6]

Giacomelli F., Wiener J., Primary myocardial disease in the diabetic mouse. An ultrastructural study, Lab Invest, 40, pp. 460-473, (1979)

[7]

Factor S.M., Minase T., Sonnenblick E.H., Clinical and morphological features of human hypertensive- diabetic cardiomyopathy, Am Heart J, 99, pp. 446-458, (1980)

[8]

Factor S.M., Bahn R., Minase T., Et al., Hypertensive- diabetic cardiomyopathy in the rat: An experimental model of human disease, Am J Pathol, 102, pp. 219-228, (1981)

[9]

Fein F.S., Sonnenblick E.H., Diabetic cardiomyopathy, Prog Cardiovasc Disease, 27, pp. 255-270, (1985)

[10]

Passa P., Leblanc H., Marre M., Effects of enalapril in insulin-dependent diabetic subjects with mild to moderate uncomplicated hypertension, Diabetes Care, 10, pp. 200-204, (1987)

← 1 2 3 4 →