Sepsis worsening vascular hyporeactivity of the superior mesenteric artery in portal vein-ligated rats.

BACKGROUND Vascular hyporeactivity is observed in portal hypertensive animals and septic rats. The objective of this study was to investigate whether impairment of superior mesenteric artery vascular contractility in the portal hypertensive rat was further impaired after sepsis. METHODS Sepsis was induced by cecum ligation and puncture (CLP) in male portal hypertensive Sprague-Dawley rats that had been subjected to portal vein ligation (PVL) for 14 days. Hemodynamic studies, isolated vascular ring studies, microbiological studies, and plasma nitrite/nitrate measurements were performed 2, 6, and 18 hours after CLP. An additional group of PVL rats received prophylactic imipenem (10 mg intravenously for 1 hour) before CLP and then were studied 6 hours after CLP. RESULTS Mean arterial pressure and heart rate of PVL rats were significantly decreased shortly after CLP. CLP caused further nitric oxide production and vascular hyporesponsiveness 6 and 18 hours after CLP compared with the baseline portal hypertensive group. Vascular hyporeactivity was corrected by N-nitro-L-arginine methyl ester + 1400W (1400W is N-(3-(aminomethyl)benzyl)acetamidine hydrochloride, a selective inducible nitric oxide synthase inhibitor). Prophylactic imipenem did not alter nitric oxide production or vascular contractility after sepsis induced by CLP. CONCLUSION Our study showed that vascular contractility in portal hypertensive rats is further impaired soon after CLP-induced sepsis.