DOSE-RESPONSE RELATIONSHIP OF ISOFLURANE AND HALOTHANE VERSUS CORONARY PERFUSION PRESSURES - EFFECTS ON FLOW REDISTRIBUTION IN A COLLATERALIZED CHRONIC SWINE MODEL

The authors studied the redistribution of myocardial blood flow in a collateral-dependent (CD) zone as a function of coronary perfusion pressure (CPP) during isoflurane and halothane anesthesia. A swine model with CD myocardium distal to a chronically occluded left anterior descending coronary artery was developed and studied. Sixteen piglets were allowed to grow for 8-10 weeks after banding of the left anterior descending coronary artery. They were randomly anesthetized with either isoflurane (n = 8) or halothane (n = 8) as the sole anesthetic, which was used to regulate specific CPP. The resultant regional myocardial blood flows were measured using radiolabeled microspheres. Four randomly allocated CPPs, of 30, 40, 45, and 55 mmHg, were studied in each animal. Four additional collateralized animals were anesthetized with alpha-chloralose, and the same CPPs were obtained using an intravenous adenosine infusion (1-5-mu-M kg-1) to validate this model. There was a proportional decrease in heart rate and blood pressure in both the isoflurane and and the halothane group with CPP. Cardiac output was significantly decreased in the halothane group at 30 mmHg when compared to 55-mmHg CPP, but it was maintained in the isoflurane group. Systemic vascular resistance was significantly lower in the isoflurane group at 30 and 40 mmHg when compared to 55-mmHg CPP. Both the isoflurane and the halothane group showed a proportional and significant decrease in endo-, mid-, and epicardial blood flows at 30-mmHg CPP when compared to baseline. In both CD and normal perfusion zones, isoflurane consistently sustained a higher endocardial blood flow than halothane (5.7-41.1%). Although both anesthetics minimally affect coronary vascular resistance, isoflurane appears to be a relatively more potent coronary vasodilator than halothane over the CPPs studied. No significant intercoronary or transmural redistribution of blood flow was present with either anesthetic at any decrement of CPP. Intravenous adenosine was a definite positive control, causing significant intercoronary and transmural coronary steal from CD endocardial regions in a dose-response fashion. The authors conclude that neither isoflurane nor halothane as the sole anesthetic in clinical concentrations causes significant coronary vasodilation or coronary steal from 55 to 30 mmHg CPP in a swine model of chronic coronary occlusion with collateral development.