[Changes in Ca++-ATPase activity of rat myocyte under cardioplegia].
Ischemic changes of cardiac muscle under cardioplegia must be evaluated at a subcellular level from functional aspects using cytochemical procedures as well as from morphological aspects. In this study, kinetics of Ca++-ATPase activity of rat cardiac myocytes under GIK-cardioplegia was estimated using a new one-step lead citrate method reported by Ando et al. The Ca++-ATPase activity of mitochondria in myocytes which had temporally increased at 15 minutes after initiation of cardioplegia, showed a slight decrease at 30 minutes and then almost disappeared at 60 minutes. At 60 minutes after the cardioplegia, the Ca++-ATPase activities of the sarcoplasmic reticula and myofilaments were well preserved and electromicroscopic findings of the myocytes remained normal. Thus, changes of Ca++-ATPase activity of mitochondria are considered to reflect ischemic damage of myocyte sharply, proceeding morphological changes in ultrastructure.
D008841:Actin Cytoskeleton / Q000201:enzymology; D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D005947:Glucose / Q000008:administration & dosage; D006324:Heart Arrest, Induced; D007328:Insulin / Q000008:administration & dosage; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000201:enzymology*; D009206:Myocardium / Q000166:cytology* / Q000648:ultrastructure; D011188:Potassium / Q000008:administration & dosage; D051381:Rats; D011919:Rats, Inbred Strains; D012519:Sarcoplasmic Reticulum / Q000201:enzymology
D007328:Insulin; C030396:glucose-insulin-potassium cardioplegic solution; D000252:Calcium-Transporting ATPases; D005947:Glucose; D011188:Potassium