Isoflurane Causes Only Minimal Increases in Coronary Blood Flow Independent of Oxygen Demand

Abstract

Studies on the coronary circulation during halothane or isoflurane anesthesia are conflicting. Also, little attention has been paid to the time course of the effect of these agents on the coronary circulation. Therefore, we investigated the direct and temporal effects of halothane and isoflurane on coronary hemodynamics in chronically instrumented dogs, in the presence and absence of autonomic nervous system blockade. On different days anesthesia was induced via inhalation with 5% halothane or isoflurane in 100% oxygen. After tracheal intubation, anesthesia was maintained at 1.0 MAC for 30 min. Hemodynamics were recorded continuously. Myocardial oxygen consumption was estimated from the pressure-work index. A total of 36 experiments (four sets of experiments) were completed using nine chronically instrumented dogs. Induction of anesthesia with halothane caused a significant (P less than 0.05) increase in coronary blood flow (from 40 +/- 6 to 68 +/- 11 ml/min), which reached a peak at 1.4 +/- 0.3 min. These changes were secondary to increases in heart rate, arterial pressure, and pressure-work index (10.2 +/- 1.4 to 15.9 +/- 0.8 ml O2.min-1.100g-1). With autonomic nervous reflexes eliminated, halothane caused no change in coronary blood flow. Inhalation of isoflurane caused a greater (P less than 0.05) increase in coronary blood flow (from 39 +/- 6 to 85 +/- 14 ml/min) than did halothane; flow reached a peak at 1.8 +/- 0.6 min. With autonomic reflexes eliminated, isoflurane continued to produce an increase (P less than 0.05) in coronary blood flow (from 39 +/- 4 to 53 +/- 5 ml/min), which reached a peak at 2.1 +/- 0.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)