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• W2091244893 abstract "Objective: We sought to determine the effects of long-term hypoxemia on fetal cardiac output and flow distribution. Study Design: We exposed six pregnant sheep to high altitude (3820 m) hypoxia from 30 to 135 days' gestation (term 146 days). Ten to 14 days after surgery we determined fetal cardiac output and organ blood flows by means of the radiolabeled microsphere technique during a baseline period and also during an additional 30-minute period of more severe added acute hypoxemia. Results: Baseline maternal arterial Po2 was 60.7 ± 1.7 torr and fell to 35.1 ± 3.0 torr during the added acute hypoxemia. Fetal arterial Po2 decreased from 18.5 ± 1.1 to 11.4 ± 1.5 torr during added acute hypoxemia. Baseline fetal cardiac output was 351 ± 55 ml/min/kg, which was significantly lower than previously reported values in low-altitude fetuses. Blood flow to critical organs such as the heart and brain was maintained at levels found in low-altitude fetuses, but flow to the carcass was significantly lower (−49%) than the mean value reported in the literature for low-altitude fetuses. Oxygen delivery was also maintained at normal levels to the brain and heart but was reduced in the kidneys (−31%), gastrointestinal tract (51%), and carcass (−58%). During added acute hypoxemia cardiac output did not change significantly; however, blood flow to the brain, heart, and adrenal glands increased 112%, 135%, and 156% (p < 0.05), respectively. Conclusion: We conclude that during long-term hypoxemia redistribution of fetal cardiac output is maintained favoring the brain and heart. Objective: We sought to determine the effects of long-term hypoxemia on fetal cardiac output and flow distribution. Study Design: We exposed six pregnant sheep to high altitude (3820 m) hypoxia from 30 to 135 days' gestation (term 146 days). Ten to 14 days after surgery we determined fetal cardiac output and organ blood flows by means of the radiolabeled microsphere technique during a baseline period and also during an additional 30-minute period of more severe added acute hypoxemia. Results: Baseline maternal arterial Po2 was 60.7 ± 1.7 torr and fell to 35.1 ± 3.0 torr during the added acute hypoxemia. Fetal arterial Po2 decreased from 18.5 ± 1.1 to 11.4 ± 1.5 torr during added acute hypoxemia. Baseline fetal cardiac output was 351 ± 55 ml/min/kg, which was significantly lower than previously reported values in low-altitude fetuses. Blood flow to critical organs such as the heart and brain was maintained at levels found in low-altitude fetuses, but flow to the carcass was significantly lower (−49%) than the mean value reported in the literature for low-altitude fetuses. Oxygen delivery was also maintained at normal levels to the brain and heart but was reduced in the kidneys (−31%), gastrointestinal tract (51%), and carcass (−58%). During added acute hypoxemia cardiac output did not change significantly; however, blood flow to the brain, heart, and adrenal glands increased 112%, 135%, and 156% (p < 0.05), respectively. Conclusion: We conclude that during long-term hypoxemia redistribution of fetal cardiac output is maintained favoring the brain and heart." @default.
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• W2091244893 date "1993-09-01" @default.
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• W2091244893 title "Effects of long-term, high-altitude hypoxemia on ovine fetal cardiac output and blood flow distribution" @default.
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• W2091244893 doi "https://doi.org/10.1016/0002-9378(93)90646-z" @default.
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