TY - JOUR
T1 - Role of O2-hemoglobin affinity in the regulation of cerebral blood flow in fetal sheep
AU - Rosenberg, A. A.
AU - Harris, A. P.
AU - Koehler, R. C.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1986
Y1 - 1986
N2 - Cerebral blood flow (CBF) and cerebral O2 transport (CBF x O2 content) in the fetal sheep are nearly twice that in the adult, despite similar rates of cerebral O2 utilization. We tested the hypothesis that the difference depends on the increased oxyhemoglobin affinity in the fetus, using P50 (PO2 at which hemoglobin is 50% saturated) as the index of oxyhemoglobin affinity. We studied 18 unanesthetized fetal sheep in utero. In six animals the P50 was raised from 16.6 ± 1.2 (SD) mmHg to 31.7 ± 4.7 mmHg by exchange transfusing the fetus with adult sheep red blood cells. We measured CBF (with radioactive microspheres) and the PO2, PCO2, pH, and O2 content in carotid artery and sagittal sinus blood twice at the original P50 and twice after exchange transfusion. Arterial O2 content fell significantly at the higher P50. Since the fall in O2 content was not accompanied by a corresponding rise in CBF, O2 transport fell by 45%. Cerebral O2 consumption (CMR(O2)) did not change and cannot be implicated in the fall of O2 transport. E (the ratio CMR(O2)/O2 transport) rose by 77%. Sham exchange transfusions in six fetuses showed that the exchange transfusion procedure itself was not responsible for this alteration. To determine whether the fall in O2 transport and the rise in E was reproducible over a range of arterial O2 contents, a third group of six fetuses was studied. Fetal arterial O2 content varied from 4 to 12 vol%, first at P50 = 17 ± 1.8 mmHg and again after exchange transfusion at P50 = 29.6 ± 3.9 mmHg. CMR(O2) was not altered at the higher P50, but O2 transport was consistently lower, and E was correspondingly higher. At each P50 level, both CMR(O2) and O2 transport were well maintained as arterial O2 content changed. In the sheep fetus the position of the oxyhemoglobin dissociation curve is an important determinant of O2 transport, but there appears to be no effect on CMR(O2) or on the ability to maintain CMR(O2) and O2 transport during isocapnic hypoxic hypoxia.
AB - Cerebral blood flow (CBF) and cerebral O2 transport (CBF x O2 content) in the fetal sheep are nearly twice that in the adult, despite similar rates of cerebral O2 utilization. We tested the hypothesis that the difference depends on the increased oxyhemoglobin affinity in the fetus, using P50 (PO2 at which hemoglobin is 50% saturated) as the index of oxyhemoglobin affinity. We studied 18 unanesthetized fetal sheep in utero. In six animals the P50 was raised from 16.6 ± 1.2 (SD) mmHg to 31.7 ± 4.7 mmHg by exchange transfusing the fetus with adult sheep red blood cells. We measured CBF (with radioactive microspheres) and the PO2, PCO2, pH, and O2 content in carotid artery and sagittal sinus blood twice at the original P50 and twice after exchange transfusion. Arterial O2 content fell significantly at the higher P50. Since the fall in O2 content was not accompanied by a corresponding rise in CBF, O2 transport fell by 45%. Cerebral O2 consumption (CMR(O2)) did not change and cannot be implicated in the fall of O2 transport. E (the ratio CMR(O2)/O2 transport) rose by 77%. Sham exchange transfusions in six fetuses showed that the exchange transfusion procedure itself was not responsible for this alteration. To determine whether the fall in O2 transport and the rise in E was reproducible over a range of arterial O2 contents, a third group of six fetuses was studied. Fetal arterial O2 content varied from 4 to 12 vol%, first at P50 = 17 ± 1.8 mmHg and again after exchange transfusion at P50 = 29.6 ± 3.9 mmHg. CMR(O2) was not altered at the higher P50, but O2 transport was consistently lower, and E was correspondingly higher. At each P50 level, both CMR(O2) and O2 transport were well maintained as arterial O2 content changed. In the sheep fetus the position of the oxyhemoglobin dissociation curve is an important determinant of O2 transport, but there appears to be no effect on CMR(O2) or on the ability to maintain CMR(O2) and O2 transport during isocapnic hypoxic hypoxia.
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U2 - 10.1152/ajpheart.1986.251.1.h56
DO - 10.1152/ajpheart.1986.251.1.h56
M3 - Article
C2 - 2425642
AN - SCOPUS:0022483126
SN - 0363-6135
VL - 251
SP - H56-H62
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 1 (20/1)
ER -