Vasodilatory Action of Propofol and the Effect of Propofol on the Contractile Response of Endotoxin Exposured Vessles in the Aortic Arteries of Rats / 대한마취과학회지

ABSTRACT

BACKGROUND: The relationship between the NO and its vasodilatory effect of propofol has been a somewhat controversial matter. And, the effects of propofol has not been evaluated in septic condition whether it is solely due to its increased iNOS activity. METHODS: First experiment is to study that the vasodilatory effect of propofol could be caused by NO. Isolated aortic rings with or without endothelium were contracted phenylephrine (10(-9)-10(-5)M) cumulatevely after porpofol (10(-5)M) administration. The effects of L-NAME (3 x 10(-4)M) and methylene blue (10(-5)M) on contractile responses for phenylephrine were evaluated. Second experiment is to study the effect of propofol on septic vesseles. the no LPS (lypopolysaccaride) and LPS treated rings with or without endothelium were contracted phenylephrine (10(-9)-10(-5)M) cumulatevely after porpofol (10(-5)M) administration. The development of sepsis was confirmed by iNOS expression using RT-PCR. RESULTS: All the aortic rings showed decreased response on phenylephrine contractile response with propofol administration. These responses were significantly less in denuded ones than in ones with intact endothelium. The endothelium dependent relaxation of propofol was inhibited by pretreatment with L-NAME and methylene blue in rat aortic rings having intact endothelium. All the aortic rings incubated with LPS showed decreased phenylephrine contractile response. The addition of propofol produced significantly more decrease in contractile response in LPS incubated rings in a greater than additive effect. The LPS induced hyporesponsiveness to phenylephrine was reversed by addition of cycloheximide. However, with the addition of propofol to LPS treated rings, complete reversal of this hyporesponsiveness to phenylephrine, failed to occur by addition of cycloheximide. CONCLUSIONS: 1) The vasodilatory effect of propofol seems to be mediatede by EDRF/NO, 2) The vasodilatory effect of propofol is increased in septic vesseles. Moreover, the inability of nitric oxide synthase inhibitior to reverse this response completely suggest that increased induction of iNOS may not be a sole responsible factor for this finding.