Critical hematocrit in intestinal tissue oxygenation during severe normovolemic hemodilution

Abstract

Background: A critical point in oxygen supply for microvascular oxygenation during normovolemic hemodilution has not been identified. The relation between organ microvascular oxygen partial pressure (μPO2) and organ oxygen consumption (V̇O2) during a decreasing oxygen delivery (DO2) is not well understood. The present study was designed to determine the systemic hematocrit and organ DO2 values below which organ μPO2 and V̇O2 cannot be preserved by regulatory mechanisms during normovolemic hemodilution. Methods: Eighteen male Wistar rats were randomized between an experimental group (n = 12), in which normovolemic hemodilution was performed with pasteurized protein solution (PPS), and a control group (n = 6). Systemic hemodynamic and intestinal oxygenation parameters were monitored. Intestinal μPO2 was measured using the oxygen-dependent quenching of palladium-porphyrin phosphorescence. Results: Baseline values in hemodilution and control group were similar. Hemodilution decreased hematocrit to 6.2 ± 0.8% (mean ± SD). Constant central venous pressure measurements suggested maintenance of isovolemia. Despite an increasing mesenteric blood flow, intestinal DO2 decreased immediately. Initially, μPO2 was preserved, whereas mesenteric venous PO2 (PmvO2) decreased; below a hematocrit of 15%, μPO2 decreased significantly below PmvO2. Critical DO2 was 1.5 ± 0.5 ml · kg-1 · min-1 for V̇O2, and 1.6 ± 0.5 ml · kg-1 · min-1 for μPO2. Critical hematocrit values for V̇O2 and μPO2 were 15.8 ± 4.6% and 16.0 ± 3.5%, respectively. Conclusions: Intestinal μPO2 and V̇O2 were limited by a critical decrease in DO2 and hematocrit at the same time. Beyond these critical points not only shunting of oxygen from the microcirculation could be demonstrated, but also a significant correlation between intestinal μPO2 and V̇O2.