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Volatile anesthetics regulate pulmonary vascular tension through different potassium channel subtypes in isolated
Renyu Liu1, Yuichi Ishibe, Naoto Okazaki
1Department of Anaesthesiology and Reanimatology, Tottori University Faculty of Medicine, Yonago, Japan. liu@mail.med.upenn.edu
Background:
The effects of volatile anesthetics on subtypes of K(+) channels located on pulmonary vessels remain largely unexplored.
Methods:
To investigate whether or not potassium channels play a role in the effect of volatile anesthetic on pulmonary vessels, isolated and perfused rabbit lungs were divided into four groups (n = 7 each): a control group without treatment, a glibenclamide (Glib) group treated with adenosine triphosphate-sensitive K(+) (K(ATP)) channel inhibitor, a 4-aminopyridine (4-AP) group treated with voltage-sensitive K(+) (K(V)) channel inhibitor, and an iberiotoxin (IbTX) group treated with high conductance calcium-activated K(+) (K(Ca)) channel inhibitor. After inhibitor administration and stabilization, two minimum alveolar concentration (MAC) of halothane, enflurane, isoflurane, or 1.8 MAC of sevoflurane were randomly administered for 15 min followed by eight minutes of fresh gas mixture after each agent inhalation.
Results:
Isoflurane did not change pulmonary vascular tension in the control group but instead constricted the pulmonary vessels when K(V) channels were inhibited with 4-AP; constrictive effects of enflurane and halothane were observed on pulmonary vessels, and were enhanced by K(V) channel inhibition with 4-AP, but they were inhibited by K(Ca) channel inhibition with IbTX; the dilation effect of sevoflurane was observed on pulmonary vessels but was not significantly affected by any of the K(+) channel inhibitors.
Conclusion:
Halothane, enflurane and isoflurane, but not sevoflurane, regulate pulmonary vascular tension through K(V) and/or K(Ca) channels in isolated rabbit lungs.