Dynamics of cardiovascular responses to repeated partial umbilical cord compression in late-gestation sheep fetus

Abstract

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 [Formula: see text] (21.1 ± 0.2 to 16.8 ± 0.2 mmHg) and a mild increase in arterial[Formula: see text] (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 2–5of 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.

Mild chronic hypoxia modifies the fetal sheep neural and cardiovascular responses to repeated umbilical cord occlusion

“…Consistent with our data, in chronically hypoxic high altitude-exposed fetal sheep with a comparable reduction in fetal arterial pO 2 and without acidosis, the bradycardic response to umbilical cord occlusion was shown not to be affected (Imamura et al, 2004). As reported by others for partial cord occlusions (Giussani et al, 1997), we observed that following the initial bradycardia fetal heart rate stabilized or even increased slightly only to fall again during the last minute of occlusion. This transient increase in heart rate parallels the increase in arterial pressure and thus may also be the result of increased sympathetic drive (Lewis et al, 1984).…”

“…The enhanced blood pressure observed in the preexisting hypoxia during the last two days of the five-day hypoxia period most likely reflects an increase in circulating catecholamines (Kitanaka et al, 1989). An elevation in plasma catecholamines elicited by chemoreceptor mechanisms is also thought to be responsible for the initial hypertension (Boekkooi et al, 1992;Cohn et al, 1974;Giussani et al, 1997). Thus, we suggest that it is possible that the difference in the initial blood pressure between control and pre-existing hypoxia group is determined by enhanced circulating catecholamines.…”

“…We applied a focused approach to the second-to-second analysis of the complex temporal profile of the fetal cardiovascular responses (Giussani et al, 1997;Matthews et al, 1990). During the first minute of occlusion the expected bradycardic response was present in both groups and no differences in the magnitude of the fall in heart rate were observed.…”

“…For clarity of presentation, Figure 1 displays 3-second averages. Data were analyzed according to (Matthews et al, 1990) as described by (Giussani et al, 1997). For each animal, we derived the minimum FHR for the first and last minute of each occlusion and we also obtained the MAP value during the hypertensive phase and during the hypotensive phase for each occlusion.…”

Effect of Maternal Fluoxetine Administration on Uterine Blood Flow, Fetal Blood Gas Status, and Growth

“…With experimental reductions in umbilical blood flow, there is fetal hypertension and bradycardia (20), whereas in the FX-exposed fetuses, there was no change in arterial pressure and tachycardia during the period of hypoxemia.…”