Propofol Attenuates Prostacyclin-induced Pulmonary Vasorelaxation in U46619 Preconstricted Dog / 대한마취과학회지

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.

Estrogen affects vascular tone differently according to vasoactive substances in ovariectomized Sprague-Dawley rat

The favorable effects of estrogen on cardiovascular diseases can be explained by several mechanisms such as changes in serum lipid profiles and thrombogenecity. Estrogen also affects the vascular tone, but there has been no report in which the effect of estrogen was tested comprehensively for several vasoactive substances, especially after long-term administration. Two weeks after bilateral ovariectomy in 8-week old female Sprague-Dawley rats, placebo or 17 beta-estradiol (E2) pellets (0.5 mg; released over 3 weeks) were implanted subcutaneously. Two weeks after pellet implantation, organ chamber experiments were performed using aortae. Compared with control, E2-treated vessels showed impaired endothelium-dependent relaxation to acetylcholine. E2 enhanced the contraction to norepinephrine and U46619 and had no effect on endothelin-1-induced contraction. In contrast, the contraction to angiotensin (AT)-II was inhibited by E2. Northern blot analysis for AT1 receptor expression using cultured aortic smooth muscle cells showed no difference between control and E2-treated cells, suggesting that AT1 receptor downregulation is not the likely mechanism. These results suggest that E2 affects the vascular tone variably according to vasoactive substances.