Published ahead of print on August 20, 2007, doi:10.1165/rcmb.2007-0081OC Am. J. Respir. Cell Mol. Biol., Volume 38, Number 2, February 2008, 135-142 A more recent version of this article appeared on February 1, 2008
Submitted on March 8, 2007 Lowering of Blood Pressure by Increasing Hematocrit with non Nitric Oxide Scavenging Red Blood CellsBeatriz Y Salazar Vazquez1,1 Faculty of Medicine, Universidad Juarez del Estado de Durango, Durango, Durango, Mexico; Department of Bioengineering, University of California, San Diego, La Jolla, CA, USA, 2 La Jolla Bioengineering Institute, La Jolla, CA, USA, 3 Department of Bioengineering, University of California, San Diego, La Jolla, CA, USA; La Jolla Bioengineering Institute, La Jolla, CA, USA, 4 Department of Bioengineering, University of California, San Diego, La Jolla, CA, USA * To whom correspondence should be addressed. E-mail: mintagli{at}ucsd.edu.
Isovolemic exchange transfusion of 40% of the blood volume (BV) in awake hamsters was used to replace native red blood cells (RBCs) with RBCs whose hemoglobin(Hb) was oxidized to methemoglobin (MetHb), MetRBCs. The exchange maintained constant BV and produced different final hematocrits (Hcts) varying from 48 to 62% Hct. Mean arterial pressure (MAP) did not change after exchange transfusion where 40% of the native RBCs where replaced with MetRBCs, without increasing Hct. Increasing Hct with MetRBCs lowered MAP by 12 mmHg when Hct was increased 12% above baseline. Further increases of Hct with MetRBCs progressively returned MAP to baseline, which occurred at 62% Hct, a 30% increase in Hct from baseline. Cardiac index (CI), increased between 2-17% above baseline for the range of Hcts tested. Peripheral vascular resistance(VR) was decreased 18% from baseline when Hct was increased 12% from baseline. VR and MAP were above baseline for increases in Hct higher than 30%. However, vascular hindrance, which reflects the contribution of vascular geometry, was lower than baseline for MetRBC, indicating prevalence of vasodilation. These suggest that acute increases in Hct with MetRBCs increase endothelium shear stress and stimulate the production of vasoactive factors (e.g. nitric oxide, NO). When MetRBCs were compared to functional RBCs, vasodilation was augmented for MetRBCs probably due to the lower NO scavenging of MetHb. Consequently, MetRBCs increased the viscosity related hypotension range compared to functional RBCs as NO shear stress vasodilation mediated responses are greater.
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