Normothermic ischaemic cardiac arrest and reperfusion of the isolated working heart: Effect of chlorpromazine on functional, metabolic and morphological recovery
The effects of chlorpromazine, an inhibitor of both Ca 2+ 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 produce...
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| Published in | Journal of molecular and cellular cardiology Vol. 15; no. 9; pp. 603 - 620 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.09.1983
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| Abstract | The effects of chlorpromazine, an inhibitor of both Ca
2+ 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 content 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. |
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| AbstractList | 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 content 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 heats (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. The effects of chlorpromazine, an inhibitor of both Ca 2+ 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 content 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. |
| Author | van der Merwe, E.L. Sanan, D. Lochner, A. van Niekerk, I. Kotzé, J.C.N. Edoute, Y. |
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2+ flux and phospholipase activity, on myocardial ultrastructure, function and metabolism were assessed... The effects of chlorpromazine, an inhibitor of both Ca2+ flux and phospholipase activity, on myocardial ultrastructure, function and metabolism were assessed... |
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| SubjectTerms | Adenosine Triphosphate - metabolism Animals Chlorpromazine - pharmacology Heart - drug effects Heart - physiopathology Heart Arrest, Induced - methods Male Mitochondria, Heart - metabolism Mitochondrial oxidative phosphorylation Mitochondrial ultrastructure Myocardium - metabolism Myocardium - ultrastructure Oxidative Phosphorylation Perfusion Phosphocreatine - metabolism Rats Rats, Inbred Strains Tissue high energy phosphates |
| Title | Normothermic ischaemic cardiac arrest and reperfusion of the isolated working heart: Effect of chlorpromazine on functional, metabolic and morphological recovery |
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