Calcium and cell death.
Irrespective of age or species, injured cardiac myocytes accumulate Ca2+. In this paper four different aspects of the Ca2+-overloading phenomenon are discussed. These aspects include the conditions under which it occurs, the possible routes of Ca2+ entry, the metabolic consequences of the raised tissue Ca2+ and possible protective procedures. The particular protective procedures that will be described involve the combined use of hypothermia and nifedipine (50 micrograms/l), with and without K+-induced chemical cardioplegia. Isolated, electrically paced rabbit hearts were made ischaemic for 60 to 180 min at 37, 28, 25, 15, 12 and 5 degrees C and then reperfused at 37 degrees C. In some experiments nifedipine was added to the perfusion buffer, with and without K+-induced cardioplegia. Recovery was assessed in terms of recovery of mechanical function, maintenance of the tissue stores of adenosine 5'-triphosphate (ATP) and creatine phosphate, and maintenance of the ATP-generating activity of the mitochondria. These results show that the cardioprotective effects of nifedipine and hypothermia are additive.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002470:Cell Survival / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism*; D006324:Heart Arrest, Induced; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D066298:In Vitro Techniques; D009206:Myocardium / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D010477:Perfusion; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits
D000255:Adenosine Triphosphate; D009543:Nifedipine; D011188:Potassium; D002118:Calcium