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1 Laboratory for Pregnancy and Newborn Research, Department of Physiology, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853-6401; 2 The Physiological Laboratory, University of Cambridge, Cambridge CB2 3EG, United Kingdom; 3 Department of Obstetrics and Gynecology, University Hospital Utrecht, 3584 CX Utrecht, The Netherlands; and 4 Pregnancy Institute, Slidel, Louisiana 70461
We characterized the detailed hemodynamics of fetal blood pressure, heart rate, common umbilical blood flow, and femoral blood flow responses to partial compression of the umbilical cord and tested the hypothesis that repeated cord compression modulates fetal cardiovascular responses in 10 chronically instrumented fetal sheep at ~130 days of gestation. In five fetuses (group I), partial compression of the umbilical cord was induced 12 times, each for 5 min at 15-min intervals. Each cord compression reduced common umbilical blood flow by 50% and produced modest falls in fetal pH (7.33 ± 0 to 7.29 ± 0) and arterial PO2 (21.1 ± 0.2 to 16.8 ± 0.2 mmHg) and a mild increase in arterial PCO2 (49.9 ± 0.5 to 54.9 ± 0.4 mmHg). Sham experiments were performed in five other fetuses (group II). Second-by-second analysis of group I fetal cardiovascular data revealed a clear biphasic response to partial cord compression. Phase I (1st min of cord compression) was characterized by a rapid bradycardia and a rapid femoral vasoconstriction (primary response); phase II (minutes 2-5 of cord compression) was characterized by a delayed bradycardia and a return of femoral vascular resistance toward baseline (secondary response). Repeated cord compression abolished the primary, but not the secondary, cardiovascular responses. These results demonstrate that fetal cardiovascular responses to stress may be modified by preexposure to repeated intrauterine challenges.
cord occlusion; biphasic response; hypoxia; mechanoreflex
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