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

This study evaluated changes in coronary blood flow (CBF), myocardial oxygen consumption (MVO(2)), and myocardial segmental shortening (SS) during intracoronary administrations of enflurane in in situ canine he arts. The left anterior descending coronary artery (LAD) of 11 anesthe tized and mechanically ventilated dogs was perfused at constant perfus ion pressure (80 mm Hg) with enflurane-free blood or with blood equili brated in an extracorporeal oxygenator with enflurane (1.1%, 2.2%, 4.4 %). CBF (measured with a Doppler flow transducer) was multiplied by th e local arteriovenous (A-V) O-2 difference to calculate MVO(2). SS was measured with ultrasonic crystals. Myocardial lactate uptake was asse ssed. Peak CBF responses during enflurane were compared with those dur ing maximum coronary vasodilation with adenosine. Enflurane caused con centration-dependent increases in CBF, and decreases in MVO(2) and SS. The greatest increase in CBF during enflurane (4.4%) was similar to t hat achievable with adenosine. Myocardial lactate uptake was not affec ted by enflurane. In conclusion, enflurane has a direct coronary vasod ilating effect. The potency of this effect is underscored by the abili ty of enflurane to cause marked increases in CBF, while appreciably re ducing myocardial O-2 demand. Since the enflurane-induced reduction in myocardial contractility was not due to ischemia, it likely reflected a direct negative inotropic effect. When the direct effects of enflur ane are compared with those of equianesthetic concentrations of haloth ane and isoflurane previously shown in the same model, enflurane has a coronary vasodilating effect similar to that of halothane but less th an that of isoflurane, and it has a negative inotropic effect greater than that of both isoflurane and halothane.