Direct coronary vasomotor effects of Sevoflurane and desflurane in in situ canine hearts

Background: An extracorporeal system was used to investigate the direct coronary vasomotor effects of sevoflurane and desflurane in vivo. The role of the adenosine triphosphate-sensitive potassium channels (K ATP channels) in these effects was evaluated. Methods: Twenty-one open-chest, anesthetized (fentanyl-midazolam) dogs were studied. The left anterior descending coronary artery was perfused at controlled pressure (80 mmHg) with normal arterial blood or arterial blood equilibrated with either sevoflurane or desflurane. Series 1 (n = 16) was divided into two groups of equal size on the basis of whether sevoflurane (1.2, 2.4, and 4.8%) or desflurane (3.6, 7.2, and 14.4%) was studied. The concentrations for the anesthetics corresponded to 0.5, 1.0, and 2.0 minimum alveolar concentration (MAC), respectively. Coronary blood flow (CBF) was measured with an ultrasonic, transit-time transducer. Local coronary venous samples were obtained and used to evaluate changes in myocardial oxygen extraction (EO 2 ). In series 2 (n = 5), changes in CBF by 1 MAC sevoflurane and desflurane were assessed before and during intracoronary infusion of the K ATP channel inhibitor glibenclamide (100 μg/min). Results: Intracoronary sevoflurane and desflurane caused concentration-dependent increases in CBF (and decreases in EO 2 ) that were comparable. Glibenclamide blunted significantly the anesthetic-induced increases in CBF. Conclusions: Sevoflurane and desflurane have comparable coronary vasodilative effects in in situ canine hearts. The K ATP channels play a prominent role in these effects. When compared with data obtained previously in the same model, the coronary vasodilative effects of sevoflurane and desflurane are similar to those of enflurane and halothane but considerably smaller than that of isoflurane.