Abstract

How the determinants of hematocrit (Hct) – alterations in mean corpuscular volume (MCV) and/or red blood cell concentration ([RBC]) – are influenced by acid–base balance adjustments across development in the chicken embryo is poorly understood. We hypothesized, based on oxygen transport needs of the embryos, that Hct will increase during 1 day of hypercapnic hypoxia (5%CO2, 15%O2) or hypoxia alone (0%CO2, 15%O2), but decrease in response to hyperoxia (0%CO2, 40%O2). Further, age-related differences in acid–base disturbances and Hct regulation may arise, because the O2 transport and hematological regulatory systems are still developing in embryonic chickens. Our studies showed that during 1 day of hypoxia (with or without hypercapnia) Hct increased through both increased MCV and [RBC] in day 15 (d15) embryo, but only through increased MCV in d17 embryo and therefore enhancement of O2 transport was age-dependent. Hypercapnia alone caused a ∼14% decrease in Hct through decreased [RBC] and therefore did not compensate for decreased blood oxygen affinity resulting from the Bohr shift. The 11% (d15) and 14% (d17) decrease in Hct during hyperoxia in advanced embryos was because of an 8% and 9% decrease, respectively, in [RBC], coupled with an associated 3% and 5% decrease in MCV. Younger, d13 embryos were able to metabolically compensate for respiratory acidosis induced by hypercapnic hypoxia, and so were more tolerant of disturbances in acid–base status induced via alterations in environmental respiratory gas composition than their more advanced counterparts. This counter-intuitive increased tolerance likely results from the relatively low M˙O2 and immature physiological functions of younger embryos.

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