title: Vascular resistance and the efficacy of red cell substitutes in a rat hemorrhage model.
abstract: We have compared polyethylene glycol-modified bovine hemoglobin (PEG-Hb; high O2 affinity, high viscosity, high oncotic pressure) and human hemoglobin cross-linked between the alpha-chains (alpha alpha-Hb; low O2 affinity, low viscosity, low oncotic pressure) with a non-O2-carrying plasma expander (pentastarch, high viscosity and oncotic pressure) after a 50% (by volume) exchange transfusion followed by a severe (60% of blood volume) hemorrhage. Mean arterial pressure and systemic vascular resistance rose significantly in the alpha alpha-Hb but not in the PEG-Hb animals. Two-hour survival was greater in the PEG-Hb animals (93%) than in control (35%), pentastarch (8%), or alpha alpha-Hb (6%) animals. In the PEG-Hb animals, there was no disturbance of acid-base balance, significantly less accumulation of lactic acid, and higher cardiac output than in the other groups. The data suggest that the rise in vascular resistance that follows alpha alpha-Hb exchange transfusion offsets the additional O2 transport provided by the cell-free hemoglobin. When resistance does not rise, as with PEG-Hb, even relatively small amounts of cell-free hemoglobin appear to be a very effective blood replacement.
authors.affiliation: Department of Medicine, School of Medicine, University of California, San Diego, and Department of Veterans Affairs Medical Center, San Diego, California 92161, USA.
authors.forename: R M
authors.initials: RM
authors.lastname: Winslow
authors.forename: A
authors.initials: A
authors.lastname: Gonzales
authors.forename: M L
authors.initials: ML
authors.lastname: Gonzales
authors.forename: M
authors.initials: M
authors.lastname: Magde
authors.forename: M
authors.initials: M
authors.lastname: McCarthy
authors.forename: R J
authors.initials: RJ
authors.lastname: Rohlfs
authors.forename: K D
authors.initials: KD
authors.lastname: Vandegriff
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001802:Blood Substitutes / Q000627:therapeutic use*; D001809:Blood Viscosity / Q000187:drug effects / Q000502:physiology; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology; D005078:Exchange Transfusion, Whole Blood; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006470:Hemorrhage / Q000503:physiopathology* / Q000628:therapy*; D019344:Lactic Acid / Q000097:blood; D008297:Male; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects* / Q000502:physiology*
chemical_list: D001802:Blood Substitutes; D019344:Lactic Acid