Oxygen lack and autonomic nervous control of the foetal circulation in the lamb

Abstract

Tying the umbilical cord in the mature foetal lamb causes an abrupt increase of blood pressure and a large decrease in heart rate (Barcroft, 1946). As Barcroft was well aware, this procedure not only removes the normal channel of gaseous exchange from the foetus, and thus (in the absence of pulmonary ventilation) induces acute asphyxia, but also causes a profound circulatory disturbance, because more than half the output of the foetal heart normally passes through the placenta. Tying the cord, therefore, cannot give a reliable indication of the response of the foetus in utero to oxygen lack alone. In this paper the effect of oxygen lack has been investigated in lambs delivered by Caesarean section by supplying the ewe with a gas mixture of low oxygen content. The immediate effect was to cause a rise of foetal blood pressure and heart rate, provided that the foetal arterial 02 saturation did not fall too rapidly or too low. Very immature lambs did not react in this way. METHODS Experiments were performed on lambs of from 59 to 143 days gestation age, from ewes of Clun-Hampshire, Suffolk or Kerry Hill breeds. The methods employed were usually the same as in the preceding paper (Dawes, .The more mature lambs were removed from the amniotic sac and the blood pressure was recorded from a femoral artery. In some younger lambs, weighing 45-100 g, the uterus was opened and the amniotic sac was exposed intact. A fine needle, attached to a condenser manometer, was introduced into one umbilical artery through the foetal membranes. There was no appreciable leak of fluid from the amniotic sac, and the umbilical artery did not go into spasm. Blood could be seen flowing past the needle tip within the artery, and the preparation remained in good condition for an hour or more.The trachea of the ewe was cannulated, and gas mixtures of varying oxygen content were delivered through calibrated rotameters.In some unanaesthetized ewes blood samples (0-8 ml.) were withdrawn under local procaine anaesthesia by direct puncture of a carotid artery. The ewes were then anaesthetized with pentobarbitone and samples were taken from a catheter passed a few cm up a median malleolar artery, and from a catheter in the left carotid artery of the foetus. In the smaller foetuses the total quantity of blood withdrawn was kept as small as possible, though in two foetuses of less than 300 g weight it exceeded 1% of the body weight. The samples were mixed with a trace of heparin

Vasomotor responses in the hind limbs of foetal and new‐born lambs to asphyxia and aortic chemoreceptor stimulation

“…It seems likely that the aortic chemoreceptors discharge continuously in some foetal lambs near term or in others in which the arterial Po2 and pH have fallen and Pe,02 has risen. This could well explain the surprisingly large fall in arterial pressure on cutting the vagi near term (Born et al 1956), a fact which was so reminiscent of the similar phenomenon in adult cats subjected to haemorrhage (Pavlov, 1879;McDowall, 1925;Kenney & Neil, 1951;Landgren & Neil, 1951) that it was one of the starting-points of the present investigation. It would also explain the femoral vasodilatation observed on vagotomy in foetal lambs near term.…”

“…Injection of the same doses of cyanide into a jugular vein, the right ventricle, pulmonary or common carotid arteries of foetal lambs caused INTRODUCTION It was concluded from previous observations that the foetal circulation might well be under effective reflex control by systemic arterial chemoreceptors (Campbell, Dawes, Fishman & Hyman, 1967 a). Since cervical vagotomy caused a fall in arterial pressure near term (Reynolds, 1954;Dawes, Mott & Rennick, 1956;Born, Dawes & Mott, 1956), and the observations of Snyder & Rosenfeld (1937), Barcroft & Karvonen (1948) and Purves & Biscoe (1966) suggested that the carotid chemoreceptors were relatively inactive, it seemed possible that the aortic chemoreceptors might be involved.…”

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

“…In the mature foetal lambn hypoxia, hypercapnia and asphyxia all cause severe pulmonary vasoconstriction both before and after ventilation of the lungs (Dawes & Mott, 1962;Cook, Drinker, Jacobson, Levison & Strang, 1963;Cassin, Dawes, Mott, Ross & Strang, 1964). This is, in part at least, by a local action, since in the isolated perfused preparation changing the gas used for positive pressure ventilation from N2 to air caused an increase in pulmonary flow at a decreased perfusion pressure (Born, Dawes & Mott, 1956). Cook et al (1963) ventilated the left lung of mature foetal lambs in vivo independently of the right lung (which was supplied with 100 % 02) and found that hypoxia or hypercapnia caused pulmonary vasoconstriction with changes in arterial 02 saturation of 0-21 % and in PCO2 of 1-6 mm Hg.…”

“…8) and increases towards term (Born et al 1956). Stimulation of the left sympathetic branches which arise from T 3-5 causes a large increase of heart rate at term (Waites, 1957;Colebatch et al 1965), but only a doubtful increase at 90 days.…”

“…Previous experiments had shown that in foetal lambs of less than 95 days gestation age hypoxaemia caused no rise in blood pressure (although there was an increase in heart rate) and injection of hexamethonium did not cause a fall in blood pressure, unlike mature foetal lambs (Born et al 1956). At this age, although asphyxia caused liberation of catecholamines (mainly noradrenaline) from the adrenal, the amount liberated was much less than at term (Comline & Silver, 1961).…”