Pulmonary vasoconstriction and changes in heart rate during asphyxia in immature foetal lambs

Abstract

The effect of changing the composition of pulmonary arterial blood on the pulmonary vasoconstrictor response to asphyxia was studied in immature fetal lambs of[long dash]90 days gestation age. When normal fetal carotid arterial blood (withdrawn before asphyxia) was introduced during asphyxia, the pulmonary vasoconstriction was rapidly and wholly relieved as soon as this blood reached the lung. This did not happen when blood was used which had been withdrawn during asphyxia. Conversely introduction into a pulmonary artery of a fetal lamb during recovery, of arterial blood withdrawn during asphyxia, caused an immediate return of pulmonary vasoconstriction. These phenomena could not be explained by the generation of vasodilator agents such as bradykinin, acetylcholine, histamine or isoprenaline. During asphyxia injection of normal fetal arterial blood into the left atrium did not caude pulmonary vasodilation, but did elicit a large increase in heart rate. Neither the pulmonary vasoconstriction during asphyxia, nor its relief by normal fetal arterial blood, nor the changes in heart rate were affected by previous bilateral vagotomy or adminis -tration of atropine or hexamethonium. It was concluded that, in immature fetal lambs, the effect of asphyxia in causing pulmonary vasoconstriction was mainly, if not exclusively, by a local action within the lungs, and that the bradycardia during asphyxia was mainly due to the fall in P02 [oxygen pressure] acting locally upon the heart.