CARDIOPROTECTIVE EFFECTS OF AMLODIPINE ON ISCHEMIA AND REPERFUSION IN 2 EXPERIMENTAL-MODELS

被引:7
作者
HOFF, PT [1 ]
TAMURA, Y [1 ]
LUCCHESI, BR [1 ]
机构
[1] UNIV MICHIGAN, SCH MED, DEPT PHARMACOL, M6322 MED SCI BLDG 1, ANN ARBOR, MI 48104 USA
关键词
D O I
10.1016/0002-9149(90)90570-Q
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The cardioprotective effect of amlodipine, a longacting dihydropyridine derivative, was studied in 2 experimental models of ischemia and reperfusion. Isolated and blood-perfused feline hearts were made globally ischemic for 60 minutes and then reperfused for 60 minutes. Alterations of left ventricular developed pressure and compliance were monitored in both amlodipine-treated hearts and salinetreated control animals. Changes in perfusion pressure indicated that amlodipine significantly reduced myocardial oxygen consumption and coronary vascular resistance. Furthermore, a progressive increase in resting left ventricular diastolic pressure indicated that amlodipine, administered before the onset of global ischemia, attenuated the development of ischemic contracture. Return of contractile function 60 minutes after reperfusion and maintenance of tissue concentrations of electrolytes were significantly better in the amlodipinetreated group than in the control animals. In intact canine hearts, regional myocardial ischemia was induced for 90 minutes, followed by 6 hours of reperfusion. Although the hemodynamic variables and the size of the region of risk did not differ significantly between treated animals and control animals, the infarct size was significantly smaller in the amlodipine-treated group than in the control animals, and a gradual reduction in coronary blood flow was observed in the control group that was prevented in the amlodipine group. A comparison of these findings with those observed with oxygen radical scavengers also is discussed. A detailed report of these studies was published in The American Journal of Cardiology (1989;64:101I-116I). This review is included here to maintain continuity of the symposium for the convenience of the reader. © 1990.
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页码:H10 / H16
页数:7
相关论文
共 49 条
[1]  
ASANO M, 1982, J PHARMACOL EXP THER, V220, P191
[2]   MARKED REDUCTION OF FREE-RADICAL GENERATION AND CONTRACTILE DYSFUNCTION BY ANTIOXIDANT THERAPY BEGUN AT THE TIME OF REPERFUSION - EVIDENCE THAT MYOCARDIAL STUNNING IS A MANIFESTATION OF REPERFUSION INJURY [J].
BOLLI, R ;
JEROUDI, MO ;
PATEL, BS ;
ARUOMA, OI ;
HALLIWELL, B ;
LAI, EK ;
MCCAY, PB .
CIRCULATION RESEARCH, 1989, 65 (03) :607-622
[3]  
BORGERS M, 1988, ANN NY ACAD SCI, V522, P433
[4]   THE EFFECTS OF VERAPAMIL, QUIESCENCE, AND CARDIOPLEGIA ON CALCIUM EXCHANGE AND MECHANICAL FUNCTION IN ISCHEMIC RABBIT MYOCARDIUM [J].
BOURDILLON, PD ;
POOLEWILSON, PA .
CIRCULATION RESEARCH, 1982, 50 (03) :360-368
[5]   ALTERED CALCIUM HOMEOSTASIS IN THE PATHOGENESIS OF MYOCARDIAL ISCHEMIC AND HYPOXIC INJURY [J].
BUJA, LM ;
HAGLER, HK ;
WILLERSON, JT .
CELL CALCIUM, 1988, 9 (5-6) :205-217
[6]  
BUJA LM, 1984, PHYSL PATHOPHYSIOLOG, P43
[7]  
BURGES R A, 1985, British Journal of Pharmacology, V85, p281P
[8]   EFFECTS OF DILTIAZEM ON EXTENT OF ULTIMATE MYOCARDIAL INJURY RESULTING FROM TEMPORARY CORONARY-ARTERY OCCLUSION IN DOGS [J].
BUSH, LR ;
ROMSON, JL ;
ASH, JL ;
LUCCHESI, BR .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1982, 4 (02) :285-296
[9]  
BUSH LR, 1981, J PHARMACOL EXP THER, V218, P653
[10]   IMPAIRED SARCOLEMMAL MEMBRANE-PERMEABILITY IN REPERFUSED ISCHEMIC MYOCARDIUM - ULTRASTRUCTURAL TRACER STUDY [J].
CAMILLERI, JP ;
JOSEPH, D ;
AMAT, D ;
FABIANI, JN .
VIRCHOWS ARCHIV A-PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY, 1980, 388 (01) :69-76