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• W2300531588 abstract "The alterations in O 2 extraction in hemodilution have been linked to fast red blood cell (RBC) velocity, which might affect the complete release of O 2 from Hb. Fast RBC velocity might also explain the normal mucosal-arterial Pco 2 (ΔPco 2 ). Yet sublingual and intestinal microcirculation have not been completely characterized in extreme hemodilution. Our hypothesis was that the unchanged ΔPco 2 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 O 2 consumption (V̇o 2 ) were targeted. Microcirculation was assessed by videomicroscopy, intestinal ΔPco 2 by air tonometry, and V̇o 2 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/mm 2 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/mm 2 and 544 ± 26 vs. 686 ± 70 μm/s, P < 0.01), and were associated with lower intestinal fractional O 2 extraction (0.61 ± 0.04 vs. 0.79 ± 0.02, P < 0.01) but preserved ΔPco 2 (5 ± 2 vs. 25 ± 4 mmHg, P < 0.01). Therefore, alterations in O 2 extraction in hemodilution seemed related to microvascular shunting, not to fast RBC velocity. The severe microvascular abnormalities suggest that normal ΔPco 2 was not dependent on CO 2 washout by the villi microcirculation. Increased perfusion in deeper intestinal layers might be an alternative explanation." @default.
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• W2300531588 date "2016-05-15" @default.
• W2300531588 modified "2023-10-14" @default.
• W2300531588 title "Intestinal and sublingual microcirculation are more severely compromised in hemodilution than in hemorrhage" @default.
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• W2300531588 doi "https://doi.org/10.1152/japplphysiol.00007.2016" @default.
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