Fetal breathing, sleep state, and cardiovascular responses to graded anemia in sheep

Abstract

Graded anemia was produced for 2 h in 10 unanesthetized fetal sheep by infusing plasma in exchange for fetal blood. This reduced the mean fetal hematocrits during the 1st h of anemia to 19.7 +/- 0.5% [control (C) = 28.2 +/- 1.1%] for mild anemia, 17.4 +/- 0.9% (C = 30.0 +/- 1.1%) for moderate anemia, and 15.1 +/- 1.0% (C = 29.2 +/- 1.3%) for severe anemia. The respective mean arterial O2 contents (CaO2) were 4.46 +/- 0.20, 3.89 +/- 0.24, and 3.22 +/- 0.19 ml/dl. Mean arterial PO2 was reduced significantly (by 2 Torr) only during moderate anemia, and mean arterial pH was decreased only during severe anemia. No significant changes occurred in arterial PCO2. Fetal tachycardia occurred during anemia. Mean arterial pressure was reduced by 2-3 mmHg during mild anemia; however, no significant blood pressure changes were observed for moderate or severe anemia. The incidence of rapid-eye movements and breathing activity was not affected by mild anemia, but the incidence of both was reduced significantly during moderate and severe anemia. It is concluded that 1) a reduction in CaO2 of greater than 2.48 +/- 0.22 ml/dl by hemodilution inhibits rapid-eye movements and breathing activity, and 2) the PO2 signal for inhibition does not come from arterial blood but from lower PO2 in tissue.

Goat Fetuses Disconnected from the Placenta, but Reconnected to an Artificial Placenta, Display Intermittent Breathing Movements

“…However, the value is not lower than that of chronically catheterized fetuses [19], which are most widely used as experimental models in fetal physiological studies. Moreover, it has been reported that fetal breathing activity was not affected by mild anemia [20]. Therefore, it is unlikely that the incidence of breathing movements is affected by the low hemoglobin concentration in this study.…”

Does fetal growth restriction induce neuropathology within the developing brainstem?

“…Preclinical studies provide evidence for a brainstem‐mediated response to acute hypoxia in utero resulting in a reduction in fetal breathing movements, a reduction in fetal heart rate and centralisation of combined cardiac output mediated by increased peripheral vascular resistance (Bartelds et al., 1993 ; Boddy et al., 1974 ; Giussani et al., 1993 ; Itskovitz et al., 1991 ; Koos et al., 1987 ). The role of the brainstem in this adaptive hypoxic response has been elucidated in fetal sheep studies in which the brainstem was transected (Dawes et al., 1983 ); without a functional brainstem, late‐gestation fetal sheep increased fetal breathing movements and nuchal muscle activity in response to an acute hypoxic episode (Dawes et al., 1983 ).…”

Hypoxia: Animal experiments and clinical implications

“…The oxygen content is reduced by decreasing the fetal hematocrit level. Isovolemic anemia is produced by an exchange transfusion method in which maternal plasma is infused into the fetal vein while simultaneously withdrawing the same volume of fetal blood from the fetal artery Hypobaric high‐altitude hypoxia.…”