Thermally induced myocardial preservation and necrosis in deprived fetal mouse hearts.
Cultured fetal mouse hearts deprived of oxygen and glucose were used to examine the effect of temperature on the mechanical, biochemical, and ultrastructural responses of the deprived myocardium to assess the utility of this in vitro model for studying myocardial necrosis, preservation, and repair. After 4 h of deprivation at 4, 24, 37, or 42 degrees C, 1) beating had ceased;2) ATP levels were decreased by 22% for 4 degrees C insults, 69% for 24 degrees C, 89% for 37 degrees C, and 97% for 42 degrees C; 3) CPK and LDH levels were unchanged; and 4) ultrastructural changes were observed. After 24 h of recovery from deprivation, 1) beating resumed, except for 42 degrees C;2) ATP levels were 102% of control for 4 degrees C; 99% for 24 degrees C; 62% for 37 degrees C; and 4% for 42 degrees C; 3) LDH content was decreased by 0% at 4 degrees C; 6% at 24 degrees C; 35% at 7 degrees C; and 70% at 42 degrees C; and 4) CPK content decreased similarly. Hypothermia protected deprived myocytes while hyperthermia accelerated cell necrosis. Combining deprivation with thermal insult in this in vitro model provides a spectrum of myocardial damage for studying the effect of interventions on repair processes and on metabolic changes in jeopardized myocardium.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D005260:Female; D005318:Fetal Heart / Q000201:enzymology / Q000503:physiopathology / Q000648:ultrastructure; D005947:Glucose / Q000378:metabolism; D006358:Hot Temperature; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D009336:Necrosis / Q000209:etiology*; D009924:Organ Culture Techniques; D010101:Oxygen Consumption; D011247:Pregnancy; D013696:Temperature; D014021:Tissue Preservation
D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D005947:Glucose