title: Sepsis decreases the spontaneous and agonist-induced contractile activities in the rat portal vein.
abstract: OBJECTIVE
  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.
authors.affiliation: Clinique d'Urologie and Division d'Hépatologie et de Gastro-entérologie, H pital Cantonal Universitaire de Genève, Switzerland.
authors.forename: D
authors.initials: D
authors.lastname: Mastrangelo
authors.forename: J L
authors.initials: JL
authors.lastname: Frossard
authors.forename: A
authors.initials: A
authors.lastname: Hadengue
authors.forename: C M
authors.initials: CM
authors.lastname: Pastor
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001424:Bacterial Infections / Q000503:physiopathology*; D008297:Male; D015287:Neurokinin B / Q000494:pharmacology*; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D009638:Norepinephrine / Q000494:pharmacology*; D011169:Portal Vein / Q000187:drug effects* / Q000503:physiopathology*; D011453:Prostaglandins / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D011453:Prostaglandins; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009569:Nitric Oxide; D015287:Neurokinin B; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat; D009638:Norepinephrine