OBJECTIVE: The study was undertaken to determine to what extent a 10-minute total umbilical cord occlusion affects autoregulation of cerebral blood flow and cerebral heat production in the fetus. STUDY DESIGN: In seven chronically catheterized late-gestation fetal sheep (127-131 days' gestation), we studied fetal blood gas, hemodynamic, and thermal responses to 10-minute total umbilical cord occlusion. RESULTS: Ten-minute umbilical cord occlusion resulted in marked hypoxia/ischemia, with oxygen content decreasing from 6.5 +/- 0.4 to 0.6 +/- 0.1 vol% and lactate concentration increasing from 1.8 +/- 0.2 to 10.7 +/- 0.7 mmol/L. During this period, the fetuses showed reductions in heart rate from 163.5 +/- 3.4 to 97.1 +/- 5.4 beats/min, mean arterial pressure from 39.4 +/- 2.1 to 21.2 +/- 2.5 mm Hg, cerebral blood flow from 101.3% +/- 8.9% to 49.7% +/- 10.3%, and cerebral heat production from 95.0% +/- 6.3% to 29.6% +/- 4.8%. During cord occlusion, cerebral blood flow was pressure passive from the fourth minute onward. The reduction in cerebral heat production preceded the reduction in perfusion pressure and cerebral blood flow. Recovery of cerebral blood flow and heat production to control values was incomplete for more than 60 minutes after restoration of umbilical flow. CONCLUSION: Ten-minute total umbilical cord occlusion results in major reductions in cerebral blood flow and heat production. Autoregulation of cerebral blood flow was lost within 4 minutes of occlusion, probably as a result of hypoxia, combined with hypotension. The fact that the reduction in cerebral heat production preceded and exceeded the reduction in blood flow may suggest active down-regulation of cerebral metabolism, the mechanism of which is unclear at present.
OBJECTIVE: The study was undertaken to determine to what extent a 10-minute total umbilical cord occlusion affects autoregulation of cerebral blood flow and cerebral heat production in the fetus. STUDY DESIGN: In seven chronically catheterized late-gestation fetal sheep (127-131 days' gestation), we studied fetal blood gas, hemodynamic, and thermal responses to 10-minute total umbilical cord occlusion. RESULTS: Ten-minute umbilical cord occlusion resulted in marked hypoxia/ischemia, with oxygen content decreasing from 6.5 +/- 0.4 to 0.6 +/- 0.1 vol% and lactate concentration increasing from 1.8 +/- 0.2 to 10.7 +/- 0.7 mmol/L. During this period, the fetuses showed reductions in heart rate from 163.5 +/- 3.4 to 97.1 +/- 5.4 beats/min, mean arterial pressure from 39.4 +/- 2.1 to 21.2 +/- 2.5 mm Hg, cerebral blood flow from 101.3% +/- 8.9% to 49.7% +/- 10.3%, and cerebral heat production from 95.0% +/- 6.3% to 29.6% +/- 4.8%. During cord occlusion, cerebral blood flow was pressure passive from the fourth minute onward. The reduction in cerebral heat production preceded the reduction in perfusion pressure and cerebral blood flow. Recovery of cerebral blood flow and heat production to control values was incomplete for more than 60 minutes after restoration of umbilical flow. CONCLUSION: Ten-minute total umbilical cord occlusion results in major reductions in cerebral blood flow and heat production. Autoregulation of cerebral blood flow was lost within 4 minutes of occlusion, probably as a result of hypoxia, combined with hypotension. The fact that the reduction in cerebral heat production preceded and exceeded the reduction in blood flow may suggest active down-regulation of cerebral metabolism, the mechanism of which is unclear at present.