Physical stress-mediated enzyme release from calcium-deficient hearts.
The effects of physical stresses produced by transient distension of a left ventricular balloon, on myocardial creatine kinase (CK) release and cellular morphology, were studied in Langendorff perfused rat hearts at 37 degrees C. Hearts subjected to 15 or 30 min anoxia, developed anoxic contracture, but only small amounts of CK were released following ventricular distension. In contrast, when anoxic hearts in contracture were perfused with calcium-free medium for 5 min, prior to distension, there occurred a large peak of CK release immediately following inflation of the intraventricular balloon. Oxygenated hearts or hearts made anoxic, but which had not developed contracture, release little CK activity, although they were subjected to ventricular distension after a calcium-free perfusion period. Large myocardial enzyme releases were associated with morphological lesions of widely separated cells, dehiscence of intercalated disc cell junctions, and sarcolemmal membrane damage. Hearts subjected to calcium-free perfusion were abnormally susceptible to physical stress-induced myocardial enzyme release.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D003402:Creatine Kinase / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism; D008297:Male; D008854:Microscopy, Electron; D009206:Myocardium / Q000201:enzymology* / Q000648:ultrastructure; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D003402:Creatine Kinase; D002118:Calcium