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The effects of acute beta 1-blockade on fetal cardiovascular reactions during asphyxia were evaluated in 11 exteriorized sheep fetuses. Gestational age was 110-142 days. Asphyxia was induced either by ventilating the mother with low oxygen gas mixture or by mechanical reduction of placental blood flow. During asphyxia all fetuses reacted to metoprolol injection with a decrease in heart rate, myocardial contractility, cardiac output and arterial blood pressure. Five experiments resulted in irreversible fetal cardiovascular collapse. Isoprenaline was given to the fetuses during hypoxia to test the ability to further increase heart rate and activate myocardial beta-adrenoceptors. In those experiments with fetal cardiovascular demise after metoprolol, the isoprenaline injection did not result in a significant tachycardia. The surviving fetuses could increase their heart rate as a sign of a capacity to further increase the sympatho-adrenergic drive.

Progressive changes in the S-T interval of the fetal electrocardiogram (FECG) were studied in 14 lamb fetuses, acutely exteriorized and subjected to graded hypoxia. The aims of the study were to investigate whether beta-adrenoceptor stimulation and hypoxia exerted additive or potentiating effects on the FECG and several cardiovascular parameters and whether the hypoxic changes of the FECG could be blocked by beta-adrenoceptor blocking agents. The FECG changes were studied in order to correlate them with cardiovascular function, as measured by heart rate, mean arterial pressure, end diastolic pressure, maximum dP/dt and combined cardiac output, estimated by the thermodilution method, as well as with blood gases, acid base status, blood lactate and glucose. Injections of small doses (0.02 to 0.4 microg kg-1 min-1) of isoprenaline induced the same pattern of changes in the FECG as we have previously recorded during hypoxia. By increasing the isoprenaline dose an increase in the duration of the FECG changes and amplitude of the T-wave changes was obtained. Propranolol was found to completely abolish the FECG changes induced by isoprenaline, as well as by mild hypoxia. During severe hypoxia the FECG changes could not be abolished by propranolol. Our previous findings indicated that the hypoxic changes could be regarded as a sign of myocardial glycolysis. Thus, the present finding that even small doses of isoprenaline given to the fetus, initiates the same pattern of FECG changes corroborate this hypothesis.