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The exact mechanisms by which the physiologic responses of the newborn infant to conditions of asphyxia are mediated are still obscure. Moreover, it is not known which disordered parameter (i.e. hypoxia, hypercapnoea, or acidaemia) provides the stimulus for any or all of these changes.Dawes and his co-workers [3, 31 have proposed that under conditions of asphyxia in the newborn lamb, constriction of the ductus arteriosus is due to the endogenous release of sympathetic amines. The evidence for this is inferred from the resultant constriction of the ductus following the administration of adrenaline to the animal.Hypoxia is known to result in a rise in pulmonary artery pressure in both animals [6, 101, and human adults [4, 11, 151. Normally room air contains 20.9% 0,. I n newborn infants exposed for short periods (6 min) to an inspired air content of 10% O,, sufficient to cause an average 5 5 % fall in arterial 0, saturation, a significant Council of Canada. and consistent rise in pulmonary arterial pressure occurred [13]. The intermediary mechanism by which these changes in pulmonary artery pressure are mediated is not known. As it is known that the administration of adrenaline in man will result in an increase in pulmonary arterial pressure [16], it is tempting to implicate the endogenous release of catecholamines as the intermediate controlling mechanism.Adrenal medullary and peripheral sympathetic activation has been demonstrated in newborn infants. Thus, tilting in the erect position (baroreceptor response) significantly increases urinary adrenaline and noradrenaline excretion, while insulininduced hypoglycaemia results in a selective rise of adrenaline only [9]. The efficacy of a reduction in the 0, content of inspired air as a stimulus t o adrenal med-dlmysympathetic secretion is less well established (vide infra).I n a previous study in this laboratory [14] it was suggested that a reduction of the inspired air 0, content to 15% did not result in any significant changes in urinary catecholamine excretion. It may,

The chemical regulation of heat production which is now well demonstrated in rats has been first postulated to be mediated through the release of adrenaline from the adrenal medulla (MORIN 1948). Recently emphasis has been put on the possible role of noradrenaline as the mediator of the non-shivering heat production (HSIEH and CARLSON 1957). It was then felt important to study the excretion of catecholamines in rats exposed to cold, as a measure of their production.Rats of the Sprague-Dawley strain weighing 170-180 g were selected.They were kept in wire cages and exposed to a temperature of + 3" C for one month. At all times rats had access to food and water. Controls were maintained at room temperature. Catecholamines in 24 hours urine and in adrenal glands were estimated according to the method of EULER and LISHAJKO (1959). As seen in the figure rats increase their excretion of noradrenaline very rapidly on exposure to cold. The response is thus nearly maximal already in the first period of 24 hours. The noradrenaline output shows a slow decline with time, but is still four times as high as in the control group after one month in the cold. The adrenaline excretion increases gradually to a maximum in 6 to 8 days and decreases rapidly thereafter.In the adrenal glands, adrenaline was reduced 25 yo after 24 hours in the cold, followed by an increased content which persisted as long as rats were kept in the cold room. The noradrenaline content did not show any significant change.Adrenalectomized rats excreted as much noradrerialine as intact animals on exposure to cold. However, the adrenaline output in urine, although significantly increased in the cold, was lower than in the control group.