Intestinal and sublingual microcirculation are more severely compromised in hemodilution than in hemorrhage

The alterations in O₂ extraction in hemodilution have been linked to fast red blood cell (RBC) velocity, which might affect the complete release of O₂ from Hb. Fast RBC velocity might also explain the normal mucosal-arterial Pco₂ (Pco₂). Yet sublingual and intestinal microcirculation have not been completely characterized in extreme hemodilution. Our hypothesis was that the unchanged Pco₂ in hemodilution depends on the preservation of villi microcirculation. For this purpose, pentobarbital-anesthetized and mechanically ventilated sheep were submitted to stepwise hemodilution (n = 8), hemorrhage (n = 8), or no intervention (sham, n = 8). In both hypoxic groups, equivalent reductions in O₂ consumption (Vo₂) were targeted. Microcirculation was assessed by videomicroscopy, intestinal Pco₂ by air tonometry, and Vo₂ by expired gases analysis. Although cardiac output and superior mesenteric flow increased in hemodilution, from the very first step (Hb = 5.0 g/dl), villi functional vascular density and RBC velocity decreased (21.7 ± 0.9 vs. 15.9 ± 1.0 mm/mm² and 1,033 ± 75 vs. 850 ± 79 μm/s, P < 0.01). In the last stage (Hb = 1.2 g/dl), these variables were lower in hemodiution than in hemorrhage (11.1 ± 0.5 vs. 15.4 ± 0.9 mm/mm² and 544 ± 26 vs. 686 ± 70 μm/s, P < 0.01), and were associated with lower intestinal fractional O₂ extraction (0.61 ± 0.04 vs. 0.79 ± 0.02, P < 0.01) but preserved Pco₂ (5 ± 2 vs. 25 ± 4 mmHg, P < 0.01). Therefore, alterations in O₂ extraction in hemodilution seemed related to microvascular shunting, not to fast RBC velocity. The severe microvascular abnormalities suggest that normal Pco₂ was not dependent on CO₂ washout by the villi microcirculation. Increased perfusion in deeper intestinal layers might be an alternative explanation.

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