• S Itoh, K Yoshida, Y Nakamura, N Mitsuhashi, and Y Kuwabara.
• Department of Obstetrics and Gynecology, Faculty of Medicine, Juntendo University, Tokyo, Japan.
• Fetal. Diagn. Ther. 1997 Sep 1; 12 (5): 314-8.

AbstractThe purpose of this study was to assess the effects of changes in fetal PaCO2 on circulatory functions without maternal influences. In 5 goat fetuses that were incubated using an extrauterine incubation system with arteriovenous extracorporeal membrane oxygenation, fetal carotid arterial blood flow, heart rate, mean blood pressure, and serum catecholamine levels were determined under the conditions of several grades of hypercapnia without hypoxemia. The hypercapnia was induced gradually by decreasing the flow of gas to the membrane oxygenator located on the extracorporeal circulation system. Fetal arterial CO2 tension increased significantly, from 36.2 +/- 1.1 mm Hg (means +/- SE) to 82.9 +/- 6.5 mm Hg, and the pH decreased significantly, from 7.410 +/- 0.012 to 7.121 +/- 0.028, due to the hypercapnia. In all cases, the fetal carotid arterial blood flow increased significantly (from 42.2 +/- 6.2 to 52.4 +/- 6.2 ml/min). Although a slight increase was observed in the heart rate at the mild hypercapnia stage, severe hypercapnia induced bradycardia in all cases. The mean arterial pressure and rate of extracorporeal circulation were unchanged during hypercapnia. We found that cerebral blood flow increased due to hypercapnia's direct effect on the vascular system, but the response of the peripheral chemoreceptor to hypercapnia seemed to be attenuated in chronic stimulation because bradycardia was induced in chronic hypercapnia.

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