PROPRANOLOL EFFECTS ON MYOCARDIAL ULTRASTRUCTURE AND HIGH-ENERGY PHOSPHATES IN ANESTHETIZED DOGS SUBJECTED TO ISCHEMIA AND REPERFUSION

被引:21
作者
ZIEGELHOFFER, A
DAS, PK
SHARMA, GP
SINGAL, PK
DHALLA, NS
机构
[1] UNIV MANITOBA, FAC MED, DEPT PHYSIOL, DIV EXPTL CARDIOL, WINNIPEG R3E 0W3, MANITOBA, CANADA
[2] UNIV MANITOBA, ST BONIFACE, DEPT SURG, RO BURRELL LAB, WINNIPEG R2H 2A6, MANITOBA, CANADA
关键词
D O I
10.1139/y79-147
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The effects of propranolol (1-5 mg/kg) on the ultrastructure and high energy phosphate content of dog myocardium were investigated after 2 h of ischemia and 2 h of reperfusion. Two adjoining major ventricular branches of the left circumflex coronary artery were occluded to produce ischemia. Propranolol was administered intravenously just before occlusion of the coronary arteries in all the experiments. Two hours of ischemia caused structural changes and significantly reduced creatine phosphate (crP) and ATP contents, and increased AMP levels. Propranolol (5 mg/kg) had no effect on these ischemic changes. Propranolol was found to protect the myocardium from structural damage usually observed after 2 h of reperfusion. The size and number of amorphous electron-dense mitochondrial granules, which are considered to contain calcium, observed after reperfusion, were reduced in propranolol-treated animals. Stores of ATP and total nucleotides (ATP + ADP + AMP), and the ATP:AMP ratio were significantly higher in propranolol (5 mg/kg) treated dogs in comparison with the untreated controls after 2 h of reperfusion. There was, however, no difference between the CrP levels of propranolol-treated and untreated preparations. The study shows that propranolol is effective in reducing the reperfusion-dependent changes in ischemic myocardium. Reduction in the intracellular calcium overload as well as maintenance of the structural integrity of the cell, particularly that of mitochondria, may be involved in these protective effects of propranolol.
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页码:979 / 986
页数:8
相关论文
共 31 条
[1]  
BERGMEYER HU, 1963, METHODS ENZYMATIC ED, P539
[2]   MYOCARDIAL REVASCULARIZATION AFTER ACUTE INFARCTION [J].
BOLOOKI, H ;
KOTLER, MD ;
LOTTENBERG, L ;
DRESNICK, S ;
ANDREWS, RC ;
KIPNIS, S ;
ELLIS, RM .
AMERICAN JOURNAL OF CARDIOLOGY, 1975, 36 (03) :395-406
[3]   CARDIOVASCULAR EFFECTS OF ACEBUTOLOL FOLLOWING CORONARY-ARTERY OCCLUSION AND REPERFUSION IN ANESTHETIZED DOG [J].
CHERNECKI, W ;
DAS, PK ;
DHALLA, NS ;
SHARMA, GP .
BRITISH JOURNAL OF PHARMACOLOGY, 1978, 64 (02) :265-272
[4]  
DECKER RS, 1978, AM J PATHOL, V92, P1
[5]   COMPARISON OF ACTIONS OF ACEBUTOLOL, PRACTOLOL AND PROPRANOLOL ON CALCIUM-TRANSPORT BY HEART MICROSOMES AND MITOCHONDRIA [J].
DHALLA, NS ;
LEE, SL .
BRITISH JOURNAL OF PHARMACOLOGY, 1976, 57 (02) :215-221
[6]   INVOLVEMENT OF MEMBRANE SYSTEMS IN HEART-FAILURE DUE TO INTRACELLULAR CALCIUM OVERLOAD AND DEFICIENCY [J].
DHALLA, NS .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1976, 8 (09) :661-667
[7]  
DHALLA NS, 1972, MYOCARDIOLOGY, V1, P81
[8]  
FLECKENSTEIN A, 1974, MYOCARDIAL BIOL RECE, V4, P563
[9]  
FURCHGOTT RF, 1958, J PHARMACOL EXP THER, V124, P203
[10]   PROPRANOLOL-INDUCED REDUCTION OF SIGNS OF ISCHEMIC-INJURY DURING ACUTE MYOCARDIAL-INFARCTION [J].
GOLD, HK ;
LEINBACH, RC ;
MAROKO, PR .
AMERICAN JOURNAL OF CARDIOLOGY, 1976, 38 (06) :689-695