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Redistribution of intestinal microcirculatory oxygenation during acute hemodilution in pigs

¹Department of Physiology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands; ²Department of Anesthesiology, University Hospital, Duesseldorf, Germany; and ³Department of Anesthesiology, Erasmus Medical Centre, Rotterdam, The Netherlands

Submitted 10 August 2004 ; accepted in final form 6 October 2004

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 the impaired ability of erythrocytes to off-load oxygen within the microcirculation, thus yielding low tissue/plasma PO₂ but elevated microcirculatory hemoglobin oxygen (HbO₂) saturations. Alternatively, oxygen shunting may also be due to reduced erythrocyte deformability, hindering the ability of erythrocytes to enter capillaries. Anesthetized pigs underwent ANH (20, 40, 60, and 90 ml/kg hydroxyethyl starch; ANH group: n = 10; controls: n = 5). We measured systemic and mesenteric perfusion. Microvascular intestinal oxygenation was measured independently by remission spectrophotometry [microcirculatory HbO₂ saturation (µHbO₂)] and palladium-porphyrin phosphorescence quenching [microcirculatory oxygen pressure in plasma/tissue (µPO₂)]. Microcirculatory oxygen shunting was assessed as the 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. Relative mesenteric perfusion decreased (decreased mesenteric/systemic perfusion fraction). A paralleled reduction occurred in mucosal µHbO₂ (68 ± 2 to 41 ± 3%) and µPO₂ (28 ± 1 to 17 ± 1 Torr). Thus the proposed constellation indicative for oxygen off-load deficits (sustained µHbO₂ at decreased µPO₂) did not develop. A twofold increase in the HbO₂-gap indicated increasing intestinal microcirculatory oxygen shunting. Significant impairment in erythrocyte deformability developed during ANH. We conclude that reduced intestinal oxygenation during ANH is, in addition to redistribution of oxygen delivery away from the intestines, associated with oxygen shunting within the intestines. This shunting appears to be not primarily caused by oxygen off-load deficit but rather by oxygen/erythrocytes bypassing capillaries, wherein a potential contributor is impaired erythrocyte deformability.

mucosa; serosa; spectrophotometry; hemoglobin; splanchnic oxygenation

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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]