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 cardiac 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 an 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 with 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% O2-5.0% CO2). In the LAD bed, measurements of CBF were obtained with an electromagnetic flowmeter and used to calculate myocardial oxygen consumption (MVO2). Percent segmental shortening (%SS) was measured with ultrasonic crystals. Changes in CBF by HAL were compared to those during maximal vasodilation with adenosine. Separate studies (n = 5) were performed using 1.4% [1 minimum alveolar anesthetic concentration (MAC)] ISO and the findings compared to those during an equianesthetic (1.0%) concentration of HAL. HAL caused concentration-dependent increases in CBF, and decreases in MVO2 and %SS. With 2.0% HAL, the level of CBF was 50% of the maximal adenosine-induced response. At equianesthetic concentrations, HAL caused increases in CBF that were one-third of those caused by ISO, while the decreases in MVO2 and %SS caused by the drugs were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)