Heart, kidney, and intestine have different tolerances for anemia.

Organ systems do not respond uniformly to changes in systemic oxygen delivery because of global and local redistributive mechanisms. We hypothesized that progressive hemodilution would evoke a different response in the microvascular oxygenation of the heart compared with kidney and gut. To evaluate this hypothesis, we studied the effect of stepwise isovolemic hemodilution on systemic hemodynamic and oxygenation parameters as well as the relation between systemic hematocrit (Ht) and microvascular PO(2) (microPO(2)) in heart, kidney, and intestines in an anesthetized and mechanically ventilated rat model. Baseline conditions were similar in the hemodilution group and in the control group. In the hemodilution group, Ht was diminished from 46.6 +/- 3.8% to 7.0 +/- 1.8% [mean +/- standard deviation (SD)]. This group had no effect on measured hemodynamics; only when Ht fell below 10% did blood pressure start to decrease. The microPO(2) values in heart, kidney, and intestines did not respond uniformly. Renal microPO(2) (56 +/- 10 mm Hg at baseline) started to decrease at a Ht of 38.5 +/- 8.6%, whereas intestinal microPO(2) (59 +/- 6 mm Hg at baseline) did not start to decrease until Ht reached 17.4 +/- 7.1%. Finally, cardiac microPO(2) (40 +/- 6 mm Hg at baseline) decreased only in the ultimate stage of the experiment at Ht of 8.7 +/- 3.5%. Based on these observations, we conclude that the regulation of microvascular oxygenation during progressive anemia is specific for each organ system. The relation between these observations and organ function and damage needs to be determined.