(Circulation. 1995;92:423-427.)
© 1995 American Heart Association, Inc.
Articles |
From the Department of Anesthesia and Critical Care and the Department of Surgery, Beth Israel Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Dr Frank W. Sellke, Department of Surgery, Division of Cardiothoracic Surgery, Beth Israel Hospital, Dana 905, 330 Brookline Ave, Boston, MA 02215.
Background Endothelium-dependent vasodilation mediated by cGMP is known to be attenuated by the inhalational anesthetic isoflurane. The present study examines the effect of isoflurane on ß-adrenergic and cAMP-mediated vasodilation.
Methods and Results Fifty-three subepicardial coronary arteries (diameter, 103±13 µm) from Wistar rats were studied in vitro in a pressurized (40 mm Hg), no-flow state with use of optical density video detection system. After preconstriction of vessels with the thromboxane A2 analogue U46619 10-6 mol/L, concentration response curves to the nonselective ß-adrenergic agonist isoproterenol, the GS protein activator sodium fluoride, the adenylate cyclase activator forskolin, the cAMP analogue 8-Br-cAMP, or the phosphodiesterase inhibitor RO20-1724 were obtained either in the presence or absence (control) of 2% isoflurane. Relaxations to all the agents tested were significantly reduced in the presence of isoflurane compared with controls.
Conclusions Isoflurane attenuates cAMP-mediated vasodilation. The impairment appears to be distal to adenylate cyclase and is not due to enhancement of cAMP phosphodiesterase.
Key Words: vasodilation receptors, adrenergic, beta anesthesia microcirculation
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