Critical Hematocrit in Intestinal Tissue Oxygenation during Severe Normovolemic Hemodilution

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 (μPo 2 ) and organ oxygen consumption (V O2 ) during a decreasing oxygen delivery (Do 2 ) is not well understood. The present study was designed to determine the systemic hematocrit and organ Do 2 values below which organ μPo 2 and V O2 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 μPo 2 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 Do 2 decreased immediately. Initially, μPo 2 was preserved, whereas mesenteric venous Po 2 (P mv o 2 ) decreased; below a hematocrit of 15%, μPo 2 decreased significantly below P mv o 2 . Critical Do 2 was 1.5 ± 0.5 ml . kg -1 . min -1 for V O2 , and 1.6 ± 0.5 ml . kg -1 . min -1 for μPo 2 . Critical hematocrit values for V O2 and μPo 2 were 15.8 ± 4.6% and 16.0 ± 3.5%, respectively. Conclusions: Intestinal μPo 2 and V O2 were limited by a critical decrease in Do 2 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 μPo 2 and V O2 .