Why the study?
Does exposure of fetal lamb blood to glass or injection of bradykinin induce pulmonary vasodilatation?
Does exposure of fetal lamb blood to glass or injection of bradykinin induce pulmonary vasodilatation?
The study demonstrates that a bradykinin-like substance is generated in fetal lamb blood upon glass exposure, acting as a potent pulmonary vasodilator.
Supports bradykinin-like vasodilation in fetal lambs; leaves open translation to human perinatal pulmonary transition.
Exposure to glass of whole blood from anaesthetized foetal lambs (at 0.6-0.95 of term) causes the rapid development of a potent pulmonary vasodilator agent.2. The formation of the vasodilator agent on exposure to glass, its disappearance with time, and the inhibition of its production by soya bean trypsin inhibitor, suggest that it is bradykinin.3. Small doses of bradykinin ( approximately 1 ng/kg) cause pulmonary vasodilatation on close arterial injection. Neither this, nor the vasodilatation caused by glass-exposed whole blood, are affected by agents which block the vasodilator actions of acetylcholine, isoprenaline or histamine.4. Exposure of foetal plasma and/or red cells to glass rarely caused the development of a pulmonary vasodilator agent. Maternal plasma was always active. Injection of the buffy coat from foetal blood caused pulmonary vasodilatation.5. The capacity of plasma from sheep at different ages to produce kinin(s) was examined by assay on the isolated rat's uterus. In the foetus activity was very low; it increased with age.6. In adolescent lambs 5-14 weeks after birth injection of approximately 10 ng/kg bradykinin into the pulmonary artery caused only a trifling vasodilatation; this was greater when pulmonary vasoconstriction was induced by lung collapse, hypoxaemia and hypercapnia.7. The possible physiological consequences of these findings are discussed.
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Campbell et al. (1968) studied this question.
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