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Korean Journal of Anesthesiology ; : 258-264, 2003.
Article in Korean | WPRIM | ID: wpr-226258

ABSTRACT

BACKGROUND: The goal of our study was to investigate the effects of propofol anesthesia on the pulmonary vascular response to prostacyclin during U46619 precontraction in dogs. METHODS: Eight mongrel dogs were anesthetized and instrumented to measure the left pulmonary vascular pressure-flow relation, by loosely positioning a hydraulic occluder around the right main pulmonary artery and placing an electromagnetic flow probe around the left main pulmonary artery. During slowly occlusion of the right main pulmonary artery, the pressure-flow plots were measured in the left main pulmonary artery in the control and propofol-anesthetized (5.0 mg/kg plus 0.5 mg/kg/min intravenously) states at baseline, after preconstriction with the U46619, and during the cumulative intravenous administration of prostacyclin. RESULTS: Propofol had no effect on the baseline pressure-flow relation versus the control state. A lower (P <0.05) dose of U46619 was necessary to achieve the same degree of preconstriction during propofol anesthesia. The pulmonary vasodilator response to prostacyclin was markedly attenuated (P <0.05) during propofol anesthesia compared to the control state. CONCLUSIONS: These results imply that propofol directly inhibits the pulmonary vasodilatory effects of prostacyclin. However the signal transduction pathway of cyclooxygenase-induced pulmonary vasodilation requires further investigation to determine mechanisms involved.


Subject(s)
Animals , Dogs , 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid , Administration, Intravenous , Anesthesia , Epoprostenol , Magnets , Propofol , Pulmonary Artery , Pulmonary Circulation , Signal Transduction , Vasodilation
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