Early Changes in Energy Metabolism in the Myocardium Following Acute Coronary Artery Occlusion in Anesthetized Dogs

Abstract

The tissue content of energy-rich phosphates and glycolytic metabolites and the activity of myocardial enzymes were examined in the dog after producing myocardial infarction by ligating branches of the anterior descending and circumflex coronary arteries. The pattern of systolic fiber movement shown by a strain-gauge assembly differentiated ischemic from nonischemic portions of myocardium. In ischemic muscle, 30 minutes after onset of ischemia, creatine phosphate content fell from 8.0 to 1.4 / z moles/g, ATP content fell from 5.8 to 1.5 fxmo]es/g, lactate content rose tenfold, and a-glycerophosphate content rose fivefold. The content of energy-rich phosphates and glycolytic metabolites did not change much in nonischemic muscle. The activities of myocardial enzymes were assayed in extracts of tissue samples from ischemic and nonischemic muscle 5 to 120 minutes after coronary artery occlusion. The activities of aldolase, lactic dehydrogenase (LDH), glyceraldehydephosphate dehydrogenase, a-glycerophosphate dehydrogenase, malatedehydrogenase (MDH).and 6-phosphogluconate dehydrogenase did not change significantly in ischemic muscle during 2 hours of observation. In nonischemic muscle, phosphofr uctokinase activity increased 75% 5 minutes after coronary occlusion, followed by an increase in activity of isocitrate dehydrogenase, creatinephosphokinase, MDH, and LDH. The enzymatic changes in nonischemic muscle suggest metabolic changes in nonischemic muscle accompanying compensatory hyperfunction and increased energy requirements of surviving muscle. ADDITIONAL KEY WORDSmyocardial ischemia enzyme profile glycolysis energy-rich phosphates myocardial fiber shortening paradoxical systolic fiber lengthening • Previous communications from this laboratory have described the biochemical changes in heart muscle that occur from 5 hours to 10 weeks following coronary oc-

Mechanisms Contributing to Malignant Dysrhythmias Induced by Ischemia in the Cat

“…7). Furthermore, although propranolol significantly reduced the sinus rate before coronary occlusion, the alterations in systemic arterial pressure and heart rate induced by ischemia were similar in treated animals with and without VF (Table III) inhibition of changes in sinus rate, does not attenuate all efferent sympathetic nerve traffic to the heart (10, 11); (b) effects of the intramyocardial release of norepinephrine subsequent to ischemia (28) (24) and to be released with myocardial ischemia (29), did not alter the cyclic AMP levels in ischemic or nonischemic cat hearts in vivo (0.1 mM) or isolated rabbit hearts (10 nM) (Table IV) Regional adrenergic activity. In the present study, regional alterations in cyclic AMP content were utilized as a potential index of local adrenergic input.…”

Quantitative assessment of the extent of myocardial infarction in the conscious dog by means of analysis of serial changes in serum creatine phosphokinase activity

“…Myocardial injury has been assessed by analysis of tissue from animals previously subjected to coronary artery occlusion with histologic, histochemical, electron microscopic, and biochemical techniques (1,(5)(6)(7)(8)(9)(10)(11)(12). We have demonstrated that myocardial creatine phosphokinase (CPK)' depletion provides an accurate index of infarct size in the rabbit (13) and in the dog (4).…”

Pyruvate-fortified resuscitation stabilizes cardiac electrical activity and energy metabolism during hypovolemia

“…The intracellular space estimates used to calculate the phosphorylation potential were calculated as 1 -[(dry mass/wet mass) + extracellular volume], where extracellular volume was taken as 0.2 mL/g wet mass based on measurements in in situ canine myocardium [22] . Proteins in frozen myocardium were extracted in phosphate buffer [34] . Protein concentrations in the extracts were measured colorimetrically [35] with a Coomassie Plus Bradford kit (Pierce, Rockford, IL).…”