Format

Send to

Choose Destination
See comment in PubMed Commons below
J Lab Clin Med. 2000 Jun;135(6):476-83.

Preservation of intestinal microvascular Po2 during normovolemic hemodilution in a rat model.

Author information

1
Department of Anesthesiology, Academic Medical Center, University of Amsterdam, The Netherlands.

Abstract

The effect of hemodilution on the intestinal microcirculatory oxygenation is not clear. The aim of this study was to determine the effect of moderate normovolemic hemodilution on intestinal microvascular partial oxygen pressure (Po2) and its relation to the mesenteric venous Po2 (Pmvo2). Normovolemic hemodilution was performed in 13 anesthetized male Wistar rats. Systemic hemodynamic and intestinal oxygenation parameters were monitored. Intestinal microvascular Po2 was measured by using the oxygen-dependent quenching of palladium-porphyrin phosphorescence. Hemodilution decreased systemic hematocrit from 45.0% +/- 0.1% (average +/- SEM) to 24.6% +/- 1.6%. The mesenteric blood flow did not change from baseline values, resulting in a linear decrease in intestinal oxygen delivery (from 2.77 +/- 0.15 to 1.42 +/- 0.11 mLxkg(-1)xmin(-1)). The intestinal oxygen extraction ratio increased significantly from 24% +/- 1% to 42% +/- 4%. Pmvo2 decreased significantly (from 57 +/- 2 to 41 +/- 2 mm Hg), but intestinal oxygen consumption and microvascular Po2 remained unaffected. As a result, the difference between microvascular Po2 and Pmvo2 increased significantly during hemodilution. Intestinal microvascular Po2 and oxygen consumption were well preserved during moderate normovolemic hemodilution. These results might be explained by the notion of others that hemodilution induces recruitment of capillaries, resulting in redistribution of the intestinal blood flow in favor of the microcirculation, which allows a more efficient extraction of oxygen. These findings further indicate that the use of venous Po2 values as indicators of microvascular oxygenation may be misleading.

PMID:
10850647
DOI:
10.1067/mlc.2000.106459
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center