Protection of the myocardium against postischemic reperfusion damage. The combined effect of hypothermia and nifedipine.
This study tests the hypothesis that the efficacy of hypothermia as a cardiacprotective agent can be increased by adding the slow channel--blocking agent, nifedipine. Isolated, electrically paced rabbit hearts were made ischemic for 60 to 180 minutes at 37 degrees, 34 degrees, 28 degrees, 25 degrees, 15 degrees, 12 degrees, and 5 degrees C and then reperfused at 37 degrees C. Recovery was assessed in terms of recovery of mechanical function, tissue stores of adenosine triphosphate (ATP), oxidative phosphorylative and ATP-generating capacity of the mitochondria, and mitochondrial Ca2+ content. Half of the hearts received 50 micrograms/L nifedipine. The results show that the protective effects of hypothermia and nifedipine are additive.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002315:Cardiopulmonary Bypass; D006321:Heart / Q000187:drug effects*; D007036:Hypothermia, Induced; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D009543:Nifedipine / Q000494:pharmacology*; D010085:Oxidative Phosphorylation / Q000187:drug effects; D011725:Pyridines / Q000494:pharmacology*; D011817:Rabbits
D011725:Pyridines; D000255:Adenosine Triphosphate; D009543:Nifedipine; D002118:Calcium