The Direct Effects of Enflurane on Coronary Blood Flow, Myocardial Oxygen Consumption, and Myocardial Segmental Shortening in In Situ Canine Hearts

Abstract

This study evaluated changes in coronary blood flow (CBF), myocardial oxygen consumption (MVo2), and myocardial segmental shortening (SS) during intracoronary administrations of enflurane in in situ canine hearts. The left anterior descending coronary artery (LAD) of 11 anesthetized and mechanically ventilated dogs was perfused at constant perfusion pressure (80 mm Hg) with enflurane-free blood or with blood equilibrated in an extracorporeal oxygenator with enflurane (1.1%, 2.2%, 4.4%). CBF (measured with a Doppler flow transducer) was multiplied by the local arteriovenous (A-V) O2 difference to calculate MVo2. SS was measured with ultrasonic crystals. Myocardial lactate uptake was assessed. Peak CBF responses during enflurane were compared with those during maximum coronary vasodilation with adenosine. Enflurane caused concentration-dependent increases in CBF, and decreases in MVo2 and SS. The greatest increase in CBF during enflurane (4.4%) was similar to that achievable with adenosine. Myocardial lactate uptake was not affected by enflurane. In conclusion, enflurane has a direct coronary vasodilating effect. The potency of this effect is underscored by the ability of enflurane to cause marked increases in CBF, while appreciably reducing myocardial O2 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 enflurane are compared with those of equianesthetic concentrations of halothane and isoflurane previously shown in the same model, enflurane has a coronary vasodilating effect similar to that of halothane but less than that of isoflurane, and it has a negative inotropic effect greater than that of both isoflurane and halothane.

Effects of intracoronary calcium chloride on regional oxygen balance and mechanical function in normal and stunned myocardium in dogs

“…It has been shown that volatile anaesthetics decrease Ca 2+ sensitivity in rat aortic vascular smooth muscle in vitro 19 and produce coronary vasodilation directly in in situ canine hearts. 20 However, the vascular responses to calcium chloride were similar in fentanyl±midazolam-and en¯urane anaesthetized dogs in the present study ( Fig. 4).…”

“…Volatile anaesthetics have been shown to enhance recovery of postischaemic myocardium 33 and to produce coronary vasodilation directly in vivo. 20 En¯urane may have protected the myocardium against ischaemia and reperfusion injury, altering the response to calcium chloride. However, we observed that responses to calcium chloride in postischaemic myocardium were similar in en¯urane-and fentanyl±midazolam-anaesthetized groups (Fig.…”

Effects of Inotropic Drugs on Mechanical Function and Oxygen Balance in Postischemic Canine Myocardium: Comparison of Dobutamine, Epinephrine, Amrinone, and Calcium Chloride

“…Halothane may have some protective effects against ischemia and reperfusion injury of the myocardium and therefore altered the response to inotropic drugs. In addition, volatile anesthetics have been shown to directly produce coronary vasodilation in vivo (27). However, it has been demonstrated that responses to inotropic drugs under halothane anesthesia do not differ from those under fentanyl-midazolam anesthesia in postischemic myocardium in dogs (28).…”

Isoflurane and coronary heart disease

“…Gurevicius et al . [55] compared the inhalational agents' effects on coronary blood flow, myocardial oxygen consumption and myocardial segmental shortening. They found that isoflurane had a superior coronary vasodilating effect to halothane and enflurane, and that isoflurane was associated with less myocardial depression than enflurane.…”