[논문]Vascular hyporesponsiveness to vasodilators in rats with cirrhosis

Safka, V.; Moreau, R.; Gadano, A.; Lebrec, D.

doi:10.1016/S0168-8278(97)80056-6

[해외논문] Vascular hyporesponsiveness to vasodilators in rats with cirrhosis

Journal of hepatology : the journal of the European Association for the Study of the Liver, v.26 no.2, 1997년, pp.382 - 386

Safka, V. (Laboratoire d'Hemodynamique Splanchnique, Unite de Recherches de Physiopathologie Hepatique, INSERM U-24, Hopital Beaujon, ,, Clichy, France) , Moreau, R. , Gadano, A. , Lebrec, D.

Abstract ▼ AI-Helper

Background/Aims: In cirrhosis, the activation of nitric oxide and prostacyclin contributes to vasolidation, and ATP-sensitive K+ (KATP) channel activation or L-type calcium (Ca2+) channel inhibition may also play a role in this process. At the same time in cirrhosis, certain endogenous mechanisms may be stimulated which limit the influence of vasodilator mechanisms on vascular tone, thus altering vascular responses to exogenous substances such as nitric oxide donors, exogenous prostacyclin, KATP channel openers or L-type Ca2+ channel blockers. The aim of the present study was to examine the arterial depressor to these exogenous substances in normal rats and in rats with secondary biliary cirrhosis.Methods: Arterial depressor dose-response curves to nitroprusside (a nitric oxide donor, 5-60 μg . kg-1 . min-1), prostacyclin (0.5-5 μg . kg-1) and aprikalim (a KATP channel opener, 10-200 μg . kg-1) were obtained in both groups. The effects of different L-type Ca2+ channel blockers, i.e. nicardipine (a dihydropyridine, 0.02-0.5 mg . kg-1), diltiazem (a benzothiazepine, 0.5-5 mg . kg-1) and verapamil (a phenylalkylamine, 0.02-0.2 mg . kg-1 . min-1), were also studied.Results: Cirrhosis produced hyporeactivity to the arterial depressor effect of all doses of nitroprusside, the lowest dose of prostacyclin and the highest doses of aprikalim or diltiazem. Cirrhosis did not significantly change depressor responses to nicardipine or verapamil.Conclusions: Rats with cirrhosis are hyporeactive to exogenous nitric oxide, prostacyclin, KATP channel opener and benzothiapezine (an L-type Ca2+ channel blocker). Therefore, cirrhosis-induced mechanisms seem to limit the decrease in vascular tone by most vasodilators. However, these mechanisms appear to be more marked in nitric oxide vasodilation than in other vasorelaxation mechanisms.

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DOI : 10.1016/S0168-8278(97)80056-6
European Association for the Study of the Liver : 저널
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