Sepsis decreases the spontaneous and agonist-induced contractile activities in the rat portal vein

Abstract

Background/Aims: The portal vein has spontaneous and agonist-induced contractile activities and whether sepsis alters these two types of contractile activities is unknown. Methods: To study the effect of sepsis on the spontaneous contractile activity and the contractile responses to norepinephrine (NE), angiotensin II (AT II), and neurokinin B (NKB) in the rat portal vein (RPV), we performed a cecal ligature and puncture (CLP) 24 h before RPV isolation. Results: CLP decreased the spontaneous activity and induced hyporesponsiveness to AT II and NKB. The vascular failure was correlated to the severity of sepsis. In contrast, the reactivity to NE was not altered. Although inducible NO synthase was detected in RPV isolated from CLP rats, NO synthase inhibitors did not restore either the responsiveness to AT II and NKB or the spontaneous activity. Additionally, hyporesponsiveness to AT II and NKB was not modified by indomethacin. Conclusions: CLP decreases the spontaneous activity of the RPV as well as the contractile responses to AT II and NKB. The vascular failure is correlated to the severity of sepsis. The reactivity to NE is not altered in this model. Neither NO nor prostaglandins are responsible for the vascular abnormalities observed during CLP.