Abstract
Abstract: The relationship between the spontaneous hematocrit (Hct) and maternal hemodynamics and the hemodynamic effects of experimentally induced changes in this Hct were studied in the awake late-pregnant guinea pig. In animals with a relatively low Hct, cardiac output fractions and blood flows to brain and heart determined with microspheres were higher and those to kidneys lower than in animals with a relatively high Hct. The O2 flows to the kidneys and skin in the former animals were also lower. Cardiac output, heart rate, systemic blood pressure, and blood flows to the other organs, including the placenta, were not related to the Hct. Placental blood flow was found to vary in proportion to cardiac output. Both hemodilution and hemoconcentration induced changes in the cardiac output distribution and organ flows which resembled those observed in the spontaneous relation with Hct. In addition, hemodilution decreased systemic blood pressure. Both hemodilution and hemoconcentration increased placental blood flow; the magnitude of this flow increase was twice as high after hemodilution. The changes in oxygen flows after experimentally induced hemodilution and hemoconcentration appears to be directly related to the concomitant change in whole blood oxygen capacity. It is concluded that in the awake late-pregnant guinea pig, only brain, heart, and kidney perfusion vary in relation to the arterial Hct. The higher placental blood flow after isovolemic hemodilution may be a result of better blood rheology in the porous-like intervillous space of the placentas in a state of reduced systemic blood pressure. The modest rise in placental blood flow after isovolemic hemoconcentration appears to be mostly related to the methodology employed.
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Peeters, L., Verkeste, C., Saxena, P. et al. Relationship between Maternal Hemodynamics and Hematocrit and Hemodynamic Effects of Isovolemic Hemodilution and Hemoconcentration in the Awake Late-Pregnant Guinea Pig. Pediatr Res 21, 584–589 (1987). https://doi.org/10.1203/00006450-198706000-00016
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DOI: https://doi.org/10.1203/00006450-198706000-00016