title: Paracentesis-induced circulatory dysfunction: mechanism and effect on hepatic hemodynamics in cirrhosis.
abstract: OBJECTIVE
  Therapeutic paracentesis may be associated with a circulatory dysfunction, manifested by a marked increase of the plasma renin activity and plasma norepinephrine. The aim of the study was to characterize the systemic and hepatic hemodynamic changes associated with paracentesis-induced circulatory dysfunction.
  
  
  METHODS
  Changes in plasma renin, aldosterone, and norepinephrine, and in systemic and hepatic hemodynamics were assessed 1 hour and 6 days after complete mobilization of ascites in 37 patients treated by total paracentesis plus intravenous dextran-70 infusion.
  
  
  RESULTS
  Paracentesis-induced circulatory dysfunction occurred in 10 patients (renin and norepinephrine increased from 9.0 +/- 10.5 to 28.8 +/- 19.0 ng.mL-1.h-1 and from 752.0 +/- 364.0 to 1223.0 +/- 294.0 pg/mL, respectively) and was associated with significant reduction in systemic vascular resistance (-13.0% +/- 2.6%; P < 0.05) and increase in hepatic venous pressure gradient (from 19.5 +/- 1.5 to 22.5 +/- 2.4 mm Hg; P < 0.01). In the remaining 27 patients, mobilization of ascites also induced a significant but smaller reduction in systemic vascular resistance (-5.0% +/- 1.6%; P < 0.05) without significant changes in renin, norepinephrine, and hepatic venous pressure gradient.
  
  
  CONCLUSIONS
  Paracentesis-induced circulatory dysfunction is predominantly caused by an accentuation of the arteriolar vasodilation already present in untreated cirrhotic patients with ascites. The homeostatic activation of endogenous vasoactive systems may account for the increased intrahepatic vascular resistance associated with this condition.
authors.affiliation: Department of Gastroenterology, Hospital Ramón y Cajal, University of Alcalá de Henares, Medrid, Spain.
authors.forename: L
authors.initials: L
authors.lastname: Ruiz-del-Arbol
authors.forename: A
authors.initials: A
authors.lastname: Monescillo
authors.forename: W
authors.initials: W
authors.lastname: Jimenéz
authors.forename: A
authors.initials: A
authors.lastname: Garcia-Plaza
authors.forename: V
authors.initials: V
authors.lastname: Arroyo
authors.forename: J
authors.initials: J
authors.lastname: Rodés
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000097:blood / Q000502:physiology; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007668:Kidney / Q000502:physiology; D008099:Liver / Q000098:blood supply* / Q000503:physiopathology; D008102:Liver Circulation / Q000502:physiology*; D008103:Liver Cirrhosis / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D018377:Neurotransmitter Agents / Q000097:blood / Q000502:physiology; D009638:Norepinephrine / Q000097:blood / Q000502:physiology; D019152:Paracentesis / Q000009:adverse effects*; D011863:Radioimmunoassay; D012083:Renin / Q000097:blood / Q000502:physiology; D013997:Time Factors; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D018377:Neurotransmitter Agents; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012083:Renin; D009638:Norepinephrine