Inhibition of endo- and epicardial glycogenolysis by propranolol in ischemic hearts

The effect of coronary artery ligation on myocardial glyocogenolysis was studied in the endo- and epicardial layers of the left ventricle in dogs pretreated with saline or 1 mg/kg of propranolol. Coronary artery ligation was performed by ligating one of the small branches of the left anterior descending coronary artery. Even after coronary artery ligation, neither increase in phosphorylase activity nor breakdown of glycogen was observed in both layers of ischemic region of myocardium in propranolol-pretreated dogs. These results indicate that pretreatment with propranolol inhibits the increase in glycogenolysis being caused by coronary artery ligation. Propranolol howefer, did not inhibit completely the coronary artery ligation-induced increase in glucose 6-phosphate and lactate and decrease in phosphocreatine in the myocardium, especially in the endocardial layers.

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Noradrenaline content and phosphorylase activity in ischemic and non-ischemic areas o-f the heart after coronary artery ligation.

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)53504-1 ◽

1980 ◽

Vol 30 ◽

pp. 144

Author(s):

Kenji Sakai ◽

Yasushi Abiko

Keyword(s):

Coronary Artery ◽

Coronary Artery Ligation ◽

Phosphorylase Activity ◽

Noradrenaline Content ◽

Artery Ligation

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Orally administered NHE1 inhibitor cariporide reduces acute responses to coronary occlusion and reperfusion

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.276.2.h749 ◽

1999 ◽

Vol 276 (2) ◽

pp. H749-H757 ◽

Cited By ~ 14

Author(s):

Rachael A. Humphreys ◽

James V. Haist ◽

Subrata Chakrabarti ◽

Qingping Feng ◽

J. Malcolm O. Arnold ◽

...

Keyword(s):

Coronary Artery ◽

Left Ventricle ◽

Mrna Expression ◽

Interventricular Septum ◽

Terminal Deoxynucleotidyl Transferase ◽

Coronary Artery Ligation ◽

Sprague Dawley ◽

Artery Ligation ◽

Acute Responses ◽

Ischemic And Reperfusion Injury

Na+/H+exchange (NHE) mediates myocardial ischemic and reperfusion injury. We examined the effects of dietary administration of the potent and selective NHE1 inhibitor cariporide on acute responses to coronary artery ligation and reperfusion in the anesthetized rat. Male Sprague-Dawley rats received control rat chow or an identical diet containing 3 parts per million of cariporide for 1 wk before 225 min of occlusion of the left main coronary artery or 45 min of occlusion followed by 180 min of reperfusion. Hearts were excised and divided into left ventricle, right ventricle, and interventricular septum for analysis of NHE1 mRNA expression and apoptosis by staining with terminal deoxynucleotidyl transferase-mediated nick end labeling. Ischemia and reperfusion were associated with a threefold elevation in NHE1 mRNA expression in control animals that was significantly reduced in cariporide-fed rats. Cariporide reduced mortality from 26% of animals to 0%. The incidence of all arrhythmias was significantly reduced, including ventricular fibrillation (from 42 to 0%) and ventricular tachycardia (from 81 to 15%), as well as the number of ventricular premature beats (from 70 ± 12 to 17 ± 6). Cariporide moderately reduced apoptosis only in the reperfused left ventricle to values not significantly greater than those in sham-operated animals, and this was associated with a significantly higher ratio of Bcl-2 to Bax. This study suggests that NHE inhibition with dietary cariporide represents an effective management of acute postinfarction responses.

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