Effect of betamethasone on mitochondrial oxidative phosphorylation in ischemic canine myocardium.
Hemodynamics and myocardial blood flow were studied in 14 anesthetized open-chest dogs that were subjected to coronary artery occlusion followed by reperfusion. In six dogs, betamethasone was given intravenously 30 minutes before occlusion. During reperfusion, a significant increase in myocardial blood flow in nonischemic tissue was observed in the betamethasone group as compared with control (P less than 0.05). Also, the increase in myocardial blood flow in steroid-treated nonischemic tissues during reperfusion was significantly greater (P less than 0.05) than that measured in ischemic tissues in the same group. However, betamethasone failed to protect mitochondrial respiration from ischemic damage. Respiratory control indices in ischemic tissues were significantly depressed, compared with those in nonischemic tissues, even in betamethasone-treated dogs, and the degree of depression was the same in the ischemic tissues of control and treated dogs. These data suggest that betamethasone was not effective in preserving mitochondrial function in ischemia but that it increased myocardial blood flow in nonischemic tissue.
D000818:Animals; D001623:Betamethasone / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism*; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D010085:Oxidative Phosphorylation / Q000187:drug effects*
D001623:Betamethasone