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1 Department of Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Department of Anesthesiology, University Hospital, Duesseldorf, Germany
2 Department of Anesthesiology, University Hospital, Duesseldorf, Germany
3 Department of Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Department of Anesthesiology, Erasmus Medical Center, Rotterdam, The Netherlands
4 Department of Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
* To whom correspondence should be addressed. E-mail: c.ince{at}amc.uva.nl.
Acute normovolemic hemodilution (ANH) compromizes intestinal microcirculatory oxygenation, however, the underlying mechanisms are incompletely understood. We hypothesized that contributors herein include redistribution of oxygen away from the intestines, and shunting of oxygen within the intestines. The latter may be due to impaired erythrocyte's ability to offload oxygen within the microcirculation, thus yielding low tissue/plasma O2-partial pressures, but elevated microcirculatory hemoglobin O2-saturations. Alternatively, O2-shunting may also be due to reduced erythrocyte deformability, hindering erythrocytes to enter capillaries. Anesthetized pigs underwent ANH (20, 40, 60, and 90ml/kg hydroxy-ethyl-starch (ANH-group:n=10; controls:n=5). We measured systemic (Qsys) and mesenteric perfusion (Qmes). Microvascular intestinal oxygenation was measured independently by remission-spectrophotometry (microcirculatory HbO2-saturation, µHbO2) and palladium-porphyrin-phosphorescence-quenching (microcirculatory O2-pressure in plasma/tissue, µPO2). Microcirculatory O2-shunting was assessed as disparity between mucosal and mesenteric venous HbO2-saturation (HbO2-gap). Erythrocyte deformability was measured as shear stress-induced cell-elongation (LORCA®-difractometer). ANH reduced hemoglobin concentration from 8.1 to 2.2 g/dl (mean±SEM). Relative mesenteric perfusion decreased (decreased Qmes/Qsys-fraction). A paralleled reduction occurred in mucosal µHbO2 (68±2% to 41±3%) and µPO2 (28±1mmHg to 17±1mmHg). Thus, the proposed constellation indicative for O2-off-load deficits (sustained µHbO2 at decreased µPO2) did not develop. A two-fold increase in the HbO2 gap indicated increasing intestinal microcirculatory O2-shunting. Significant impairment in erythrocyte deformability developed during ANH. We conclude that reduced intestinal oxygenation during ANH is -in addition to redistribution of O2-delivery away from the intestines- associated with O2-shunting within the intestines. This shunting appears not primarily caused by O2-offload deficit, but rather by O2/erythrocytes bypassing capillaries, wherein a potential contributor is impaired erythrocyte deformability.
This article has been cited by other articles:
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  E. G. Mik, T. Johannes, and C. Ince Monitoring of renal venous PO2 and kidney oxygen consumption in rats by a near-infrared phosphorescence lifetime technique Am J Physiol Renal Physiol, March 1, 2008; 294(3): F676 - F681. [Abstract] [Full Text] [PDF]
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T. Johannes, E. G. Mik, B. Nohe, K. E. Unertl, and C. Ince Acute decrease in renal microvascular PO2 during acute normovolemic hemodilution Am J Physiol Renal Physiol, February 1, 2007; 292(2): F796 - F803. [Abstract] [Full Text] [PDF]
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