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CARDIOVASCULAR ANESTHESIOLOGY

Sevoflurane, but Not Propofol, Prevents Rho Kinase-Dependent Contraction Induced by Sphingosylphosphorylcholine in the Porcine Coronary Artery

Hiroyuki Kinoshita, MD, PhD^*, Naoyuki Matsuda, MD, PhD, Yoshiki Kimoto, MD, PhD^*, Setsuko Tohyama, MD, Keiko Hama, MD^*, Katsutoshi Nakahata, MD, PhD^*, and Yoshio Hatano, MD, PhD^*

From the *Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan; Departments of Anesthesiology and Molecular Medical Pharmacology, Toyama University School of Medicine, Toyama, Japan; and Departments of Sports Medicine and Joint Reconstruction Surgery, Hokkaido University School of Medicine, Sapporo, Japan.

Address correspondence and reprint requests to Hiroyuki Kinoshita, MD, PhD, Department of Anesthesiology, Wakayama Medical University, 811-1 Kimiidera, Wakayama, Wakayama 641-0012, Japan. Address e-mail to hkinoshi{at}pd5.so-net.ne.jp.

Abstract

BACKGROUND: Sphingosylphosphorylcholine may induce coronary vasospasm by the activation of Rho kinase. We designed the current study to examine the differential effects of anesthetics on Rho kinase activation induced by sphingosylphosphorylcholine in porcine coronary arteries.

METHODS: Rings of porcine coronary artery without endothelium were prepared in tissue bath containing modified Krebs–Ringer bicarbonate solution. Using isometric force recording, concentration–response curves in response to sphingosylphosphorylcholine were obtained in the absence or in the presence of sevoflurane, propofol, or a selective Rho kinase inhibitor Y27632, which was added 15 min before the application of sphingosylphosphorylcholine. Intracellular translocation of Rho A toward the plasma membrane and phosphorylation of the myosin-targeting subunit of myosin light chain phosphatase were also evaluated by Western blotting.

RESULTS: Sphingosylphosphorylcholine (10^–7 to 10^–5 M) produced contraction of the porcine coronary artery, which was abolished by a selective Rho kinase inhibitor Y27632 (2 x 10^–6 M). Sevoflurane (1.7%) reduced sphingosylphosphorylcholine-induced coronary artery constriction, and the higher concentration (3.4%) abolished it (P < 0.05). In contrast, propofol (3 x 10^–6 M and 10^–5 M) had no effect on coronary artery constriction due to sphingosylphosphorylcholine. Sevoflurane, but not propofol, reduced intracellular translocation of Rho A toward the plasma membrane. Sevoflurane and Y27632, but not propofol, similarly decreased (64.4% or 70.8% reduction, respectively, P < 0.05) phosphorylation of the myosin-targeting subunit of myosin light chain phosphatase.

CONCLUSIONS: Sphingosylphosphorylcholine induces coronary vasocontriction via activation of Rho kinase. Sevoflurane, but not propofol, inhibits this pathway, resulting in prevention of vasoconstriction.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999