Hemodynamic and metabolic effects of sodium nitroprusside on the performance and metabolism of regional ischemic myocardium;.
To assess the effects of sodium nitroprusside (5-10 mug/min) on total and regional cardiac performance, energetics, and lactate metabolism during acute ischemia, studies were performed in 21 open-chest dogs. For studies of regional function and metabolism, length gauges were sutured to the epicardial surface and an epicardial vein adjacent to the artery to be occluded was cannulated. Following occlusion of the left anterior descending coronary artery, cardiac output, mean arterial pressure, epicardial vein blood flow, and systolic shortening of the ischemic segment decreased significantly, In the blood samples from the ischemic zone, but not in those from the coronary sinus, lactate extraction shifted to production. In seven control dogs these alterations persisted throughout the experiment. In 14 animals treated with nitroprusside, cardiac output increased while peripheral resistance and mean arterial pressure decreased. Systolic shortening in the ischemic segment increased from 1.10 +/- 0.24 (SEM) to 1.77 +/- 0.30 mm (P less than 0.005). In eight dogs, regional venous outflow increased from 1.9 +/- 0.1 to 3.0 +/- 0.4 ml/min despite a slight reduction in mean arterial pressure. Concomitantly, regional negative lactate balance was reduced from -61.0 +/- 20.0 to -23.2 +/- 5.7% (P less than 0.05). These results indicate that nitroprusside significantly improves both total cardiac performance and the mechanical performance of regional ischemic myocardium. Moreover, this improvement in mechanical function occurred concomitantly with apparent increase in regional perfusion and reduction in lactate production, suggesting that nitroprusside simultaneously alleviates ischemia.
D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D003251:Constriction, Pathologic; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects*; D004195:Disease Models, Animal; D004285:Dogs; D005292:Ferricyanides / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects*; D007773:Lactates / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology*; D011312:Pressure; D014655:Vascular Resistance / Q000187:drug effects
D005292:Ferricyanides; D007773:Lactates; D009599:Nitroprusside