Role of adenosine triphosphate-sensitive potassium channels in coronary vasodilation by halothane, isoflurane, and enflurane

Background: Halothane, isoflurane, and enflurane cause coronary vasodilation and cardiac depression, This study was performed to assess the role of adenosine triphosphate (ATP)-sensitive potassium channels (K-ATP channels) in these effects, Methods: Twenty-five thoracotomized dogs mere anesthetized with fentanyl and midazolam. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs, One reservoir was supplied with arterial blood free of a volatile anesthetic, and the second reservoir was supplied with arterial blood equilibrated in an oxygenator with a I minimum alveolar concentration of either halothane (0.9%, n = 10), isoflurane (1.4%, n = 8), or enflurane (2.2%, n = 7). Coronary blood flow (CBF) was measured using a Doppler flow transducer, and segmental shortening (SS) was measured with ultrasonic crystals. Responses to the volatile anesthetics were assessed under control conditions, during intracoronary infusion of the K-ATP channel inhibitor glibenclamide (100 mu g/min), and after cessation of glibenclamide (recovery). The effectiveness of glibenclamide was verified from inhibition of coronary vasodilator responses to the K-ATP channel opener cromakalim without effect on those to the K-ATP channel-independent vasodilators, sodium nitroprusside and acetylcholine. Results: Under control conditions, the volatile anesthetics caused pronounced increases in CBF (isoflurane > halothane = enflurane), and decreases in SS (enflurane > halothane = isoflurane), Glibenclamide blunted significantly (and reversibly) the increases in CBF, but it had no effect on the decreases in SS. Conclusions: The K-ATP channels play an important role in coronary vasodilation but apparently are not involved in cardiac depression caused by halothane, isoflurane, and enflurane in canine hearts in situ.