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

Background/Aims: The portal vein has spontaneous and agonist-induced contra ctile activities and whether sepsis alters these two types of contractile a ctivities is unknown. Methods: To study the effect of sepsis on the spontaneous contractile activ ity and the contractile responses to norepinephrine (NE), angiotensin II (A T(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 hyporesponsiven ess 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 indu cible NO synthase was detected in RPV isolated from CLP rats, NO synthase i nhibitors did not restore either the responsiveness to AT(II) and NKB or th e spontaneous activity, Additionally, hyporesponsiveness to ATII and NKB wa s not modified by indomethacin. Conclusions: CEP decreases the spontaneous activity of the RPV as well as t he contractile responses to AT(II) and NKB. The vascular failure is correla ted to the severity of sepsis. The reactivity to NE is not altered in this model, Neither NO nor prostaglandins are responsible for the vascular abnor malities observed during CLP.