title: Late hemodynamic changes following controlled hemorrhage and volume restitution with blood or Haemaccel in anesthetized portal hypertensive rats.
abstract: OBJECTIVE
  In portal hypertensive rats, hemorrhage and acute volume restitution with Haemaccel induced increased cardiac output and portal venous inflow. In the present study, the late hemodynamic effects of this procedure were explored.
  
  
  METHODS
  Portal hypertension was induced by portal vein constriction. Blood was withdrawn 11.2 +/- 3.2 days later, at a rate of 0.3 mL/min, for 15 min, followed by 15 min of stabilization. Haemaccel or blood were infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after 24 h, using radioactive microspheres. Viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as resistance/viscosity ratio.
  
  
  RESULTS
  Blood viscosity of the Haemaccel group (n = 11), was lower than in the blood group (n = 11): 2.7 +/- 0.2 versus 4.0 +/- 0.4 (P < 0.01). Arterial pressure, cardiac output, peripheral resistance, portal pressure, portal venous inflow and splanchnic arteriolar resistance were not significantly different. Splanchnic arteriolar and portocollateral hindrance were higher in the Haemaccel group (11.7 +/- 5.3 and 1.5 +/- 0.6 vs 7.7 +/- 3.0 and 0.9 +/- 0.4 mmHg x min x 100 gram body weight/mL, respectively, P < 0.05).
  
  
  CONCLUSIONS
  In portal hypertensive rats, vital organs perfusion, 24 h after hemorrhage and isovolemic volume restitution with Haemaccel and blood, was similar. However, in Haemaccel-transfused animals, a reduction in vascular hindrance, indicating vasoconstriction, was observed in the splanchnic organs, which drain into the portal circulation. Vasoconstriction of the portocollateral vascular bed was observed as well. We suggest that slow-rate volume replacement during a portal-hypertensive-related bleeding episode enables hemodynamic adaptation to occur. Thus, undesirable hyperdynamic changes, which may aggravate secondary bleeding, are attenuated.
authors.affiliation: Liver Research Laboratory, The Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
authors.forename: Nir
authors.initials: N
authors.lastname: Hilzenrat
authors.forename: Arieh
authors.initials: A
authors.lastname: Yaari
authors.forename: Emanuel
authors.initials: E
authors.lastname: Sikuler
mesh_terms: D000818:Animals; D001769:Blood; D001809:Blood Viscosity; D001810:Blood Volume; D006471:Gastrointestinal Hemorrhage / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology*; D006975:Hypertension, Portal / Q000503:physiopathology*; D008297:Male; D011097:Polygeline / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D011097:Polygeline