Effect of sodium nitroprusside on directly measured myocardial oxygen consumption during phenylephrine-induced hypertension in dogs anesthetized with halothane.

Regional myocardial O2 consumption (MVO2) was measured directly as the product of left anterior descending coronary artery blood flow and coronary arteriovenous O2 content difference in eight dogs anesthetized with 1% halothane in O2 following thiopental induction. Changes in MVO2, brought about by infusions of phenylephrine and sodium nitroprusside, were compared with simultaneously observed changes in some readily obtainable indirect induces of MVO2 such as the tension-time index and the heart rate-blood pressure product. During halothane alone average values of mean arterial pressure and regional MVO2 were, respectively, 81 mm Hg and 3.6 ml of O2/min. When mean arterial pressure was increased to 126 mm Hg (average) and held there for 27 minutes by continuously infusing a dilute solution of phenylephrine, regional MVO2 averaged 5.4 ml/min. When mean arterial pressure was lowered to 77 mm Hg for a 36-minute period by infusing sodium nitroprusside (phenylephrine infusion maintained), regional MVO2 fell to 2.5 ml/min. There was a high and significant correlation between changes in directly measured regional MVO2 and simultaneously observed changes in mean arterial pressure, tension-time index, and heart rate-blood pressure. These results indicate that during halothane anesthesia in healthy dogs, changes in readily obtainable indirect indices of MVO2 such as the tension-time index and heart rate-blood pressure product, accurately characterize changes in MVO2 directly measured.