DIRECT EFFECTS OF HALOTHANE ON CORONARY BLOOD-FLOW, MYOCARDIAL OXYGEN-CONSUMPTION, AND MYOCARDIAL SEGMENTAL SHORTENING IN IN-SITU CANINE HEARTS

Previous in vivo studies of the coronary vascular effects of halothane (HAL) were complicated by varying hemodynamic conditions and global c ardiac work demands. Accordingly, the current study evaluated changes in coronary blood flow (CBF) and associated variables during selective intracoronary administrations of HAL in in situ canine hearts using a n extracorporeal-controlled pressure perfusion system. Findings during HAL were compared to those during isoflurane (ISO). The left anterior descending coronary artery (LAD) of 8 open-chest dogs anesthetized wi th fentanyl and midazolam was perfused at constant pressure (109 +/- 2 mm Hg) with HAL-free arterial blood or with blood equilibrated in an extracorporeal oxygenator with HAL (0.5%, 1.0%, 2.0% in 95% O-2-5.0% C O2). In the LAD bed, measurements of CBF were obtained with an electro magnetic flowmeter and used to calculate myocardial oxygen consumption (MVo(2)). Percent segmental shortening (%SS) was measured with ultras onic crystals. Changes in CBF by HAL were compared to those dur ing ma ximal vasodilation with adenosine. Separate studies (n = 5) were perfo rmed using 1.4% [1 minimum alveolar anesthetic concentration (MAC)] IS O and the findings compared to those during an equianesthetic (1.0%) c oncentration of HAL. HAL caused concentration dependent increases in C BF, and decreases in MVo(2) and %SS. With 2.0% HAL, the level of CBF w as 50% of the maximal adenosine-induced response. At equianesthetic co ncentrations, HAL caused increases in CBF that were one-third of those caused by ISO, while the decreases in MVo(2) and %SS caused by the dr ugs were not significantly different. We conclude that HAL has a direc t concentration-dependent relaxing action on vascular smooth muscle in the coronary circulation of the in situ canine heart. The ability of HAL to increase CBF significantly while it was reducing local myocardi al O-2 requirements by a direct negative inotropic effect attests to t he potency of this vasodilator action. HAL was a less potent direct co ronary vasodilator than ISO, whereas it had a comparable direct negati ve inotropic effect.