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KMID : 0858219970010040436
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Intravenous Anesthesia
1997 Volume.1 No. 4 p.436 ~ p.436
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Effect of Propofol on Induction of Nitric Oxide Synthase in Endotoxin-exposed Rat Aortic Rings
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Kim YH
Han KC/Yoon SH/Son SC/Lee JU/Choi SJ
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Abstract
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The Aim was to investigate the effects of propofol on endotoxin exposed vascular smooth muscle.
METHODS: Thoracic aortae were excised from rat and cut 7into 3mm rings. After incubationin aerated organ baths containing a modified Tris Tyrode solution with or without Escherichia coli lipopolysaccaharide(100/ml) at 37oC for 2 hrs, the rings were suspended in baths for isometric tension recording. Phenylephrine dose-response data (10 9~10 5 M) were determined for lipopolysaccaride and nonlipopolysaccsride treated rings. After washout and equirbration, two vessels were additionally exposed to propofol(10 5 M) and phenylephrine dose response determinations were repeated for all vessels. The nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester L-NANE or cycloheximide were added to the bath after washout from the second phenylephrine dose- response determination. Then, a third phenylephrine dose-response determination was performed with and without propofol.
RESULTS: Propofol resulted in a decrease in contractile response to phenylephrine in LPS and nonLPS treated vessles. The LPS treated vessels showed larger decrease in response to pheylephrine than nonLPS treated vessels. This depressed contractile response was restored signigicantly by the addition with L-NAME in with or without LPS treated vessels. And addition of cycloheximide, inducible nitric oxide synthase inhibitor resulted in decrease in vasodilatory effect of propofol on LPS treated vessels.
CONCLUSION: Exposure of rat aortic rings to lipopolysaccaride in vitro decreased the contractile response to phenylephrine. The addition of propofol resulted in a more decrease in tension in the lipopolysaccaride-treated vessels. The ability of cycloheximide to reverse this response suggests that induction of nitric oxide synthase and increased production of nitric oxide are responsible for effect of propofol on LPS exposed vessels.
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