Normothermic ischaemic cardiac arrest and reperfusion of the isolated working heart: Effect of chlorpromazine on functional, metabolic and morphological recovery
Date
1983
Authors
Edoute Y.
Van der Merwe E.L.
Sanan D.
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Abstract
The effects of chlorpromazine, an inhibitor of both Ca2+ flux and phospholipase activity, on myocardial ultrastructure, function and metabolism were assessed during normothermic ischaemic cardiac arrest and reperfusion of the isolated working rat heart. Normothermic ischaemic cardiac arrest produced significant changes in myocardial ultrastructure, high energy phosphate contents and mitochondrial oxidative phosphorylation within 20 min. Reperfusion of untreated hearts subjected to 20 and 25 min ischaemia failed to restore mitochondrial function, mechanical activity and ATP contents to control, pre-ischaemic levels. Morphological signs of ischaemic injury regressed, especially in the subendocardial layer. Pretreatment of hearts with chlorpromazine did not prevent the ischaemia-induced changes in myocardial ultrastructure and mitochondrial function. However, during reperfusion the chlorpromazine-treated, totally ischaemic hearts (20 to 25 min) exhibited improved coronary flow rates, and ultrastructural and mechanical recovery. The mitochondrial oxidative phosphorylation process and tissue high energy phosphate contents were not affected by the drug.
Description
Keywords
chlorpromazine, animal cell, animal experiment, electron microscopy, heart, heart arrest, heart function, heart muscle ischemia, heart muscle metabolism, isolated heart, nonhuman, rat, ultrastructure, Adenosine Triphosphate, Animal, Chlorpromazine, Heart, Heart Arrest, Induced, Male, Mitochondria, Heart, Myocardium, Oxidative Phosphorylation, Perfusion, Phosphocreatine, Rats, Rats, Inbred Strains
Citation
Journal of Molecular and Cellular Cardiology
15
9
15
9