title: Evolution of portal-systemic collateral vasopressin response in endotoxemic portal hypertensive rats.
abstract: Cirrhotic patients with portal hypertension and variceal hemorrhage are vulnerable to endotoxemia. However, the direct influence of endotoxemia on portal-systemic collateral vasculature remains unexplored. In this study, portal hypertension was induced in Sprague-Dawley rats by partial portal vein ligation. On the 7th day after portal vein ligation, at 0.5, 1.5, and 5 h post endotoxin (LPS; Escherichia coli serotype O111:B4, 3 mg/kg, i.p., E0.5, E1.5 and E5, respectively) or saline (control, C0.5, C1.5, and C5, respectively) injection, hemodynamic measurements and concentration-response relationships to arginine vasopressin (AVP; 10(-10)-10(-7) mol/L) in collateral vascular bed were obtained. In another six parallel groups, reverse-transcriptase-polymerase chain reaction of iNOS, eNOS, and endothelin 1 (ET-1) mRNA expressions for splenorenal shunt, the most prominent intra-abdominal collateral vessel, was performed. The results showed that E0.5 had lower perfusion pressure changes to AVP and higher splenorenal shunt eNOS expression than C0.5 group (P < 0.05). Compared with C1.5, tachycardia, higher perfusion pressure changes and enhanced splenorenal shunt iNOS and ET-1 expression were observed in E1.5 group (P < 0.05). In E5, systemic and portal hypotension with markedly enhanced collateral AVP responsiveness and splenorenal shunt iNOS and ET-1 expressions were noted (P < 0.05). In conclusion, vasoactive substances counterregulation participates, at least in part, the time-dependent changes of collateral AVP responsiveness in endotoxemic portal hypertensive rats.
authors.affiliation: Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, Taiwan, Republic of China.
authors.forename: Hui-Chun
authors.initials: HC
authors.lastname: Huang
authors.forename: Sun-Sang
authors.initials: SS
authors.lastname: Wang
authors.forename: Ching-Chih
authors.initials: CC
authors.lastname: Chang
authors.forename: Fa-Yauh
authors.initials: FY
authors.lastname: Lee
authors.forename: Han-Chieh
authors.initials: HC
authors.lastname: Lin
authors.forename: Ming-Chih
authors.initials: MC
authors.lastname: Hou
authors.forename: Tzu-Hua
authors.initials: TH
authors.lastname: Teng
authors.forename: Yi-Chou
authors.initials: YC
authors.lastname: Chen
authors.forename: Shou-Dong
authors.initials: SD
authors.lastname: Lee
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology*; D019332:Endothelin-1 / Q000235:genetics; D019446:Endotoxemia / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D006975:Hypertension, Portal; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D052247:Nitric Oxide Synthase Type II / Q000235:genetics; D052250:Nitric Oxide Synthase Type III / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D019332:Endothelin-1; D008070:Lipopolysaccharides; D014662:Vasoconstrictor Agents; D001127:Arginine Vasopressin; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III