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1. The effect of changing the composition of pulmonary arterial blood on the pulmonary vasoconstrictor response to asphyxia was studied in immature foetal lambs of 90 days gestation age.

2. When normal foetal carotid arterial blood (withdrawn before asphyxia) was introduced during asphyxia, the pulmonary vasoconstriction was rapidly and wholly relieved as soon as this blood reached the lung. This did not happen when blood was used which had been withdrawn during asphyxia.

3. Conversely introduction into a pulmonary artery of a foetal lamb during recovery, of arterial blood withdrawn during asphyxia, caused an immediate return of pulmonary vasoconstriction.

4. These phenomena could not be explained by the generation of vasodilator agents such as bradykinin, acetylcholine, histamine or isoprenaline.

5. During asphyxia injection of normal foetal arterial blood into the left atrium did not cause pulmonary vasodilatation, but did elicit a large increase in heart rate.

6. Neither the pulmonary vasoconstriction during asphyxia, nor its relief by normal foetal arterial blood, nor the changes in heart rate were affected by previous bilateral vagotomy or administration of atropine or hexamethonium.

7. It was concluded that, in immature foetal 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 P_O2 acting locally upon the heart.

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