Biomedical subjects
Publications and source records attributed to J W Ritchie.
The effect upon fetal breathing movements (FBM) in 49 women with uncomplicated pregnancies who inhaled 5% carbon dioxide in air for 15 minutes was observed with an ADR real-time ultrasound scanner. A threefold increase in FBM occurred during the inhalation of CO2.
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The effect of maternal inhalation of 50 per cent oxygen upon fetal breathing movements was investigated. No significant effect was noted in patients with normal pregnancies or in those complicated by insulin dependent diabetes or mild pre-eclampsia. A significant increase in fetal breathing movements was observed in those pregnancies complicated by either severe pre-eclampsia or fetal growth retardation.
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Fetal breathing movements (FBM) and generalized fetal movements (GFM) were recorded for 30 minutes using a real time B-scan instrument in 46 women with uncomplicated pregnancies. FBM occurred for 10.9+/-0.9 (SE) per cent of the recording time. The time occupied by FBM was not significantly related to smoking, meal times or plasma glucose concentrations. FBM were absent during the observation period in 15 per cent of patients and present for less than 10 per cent of the time in 33 per cent of patients.
1. Adrenaline and noradrenaline have been infused into the fetal sheep to produce plasma concentrations comparable to those seen during hypoxia and the cardiovascular changes compared with those seen in response to hypoxia. The effect of isoprenaline, methoxamine, and beta- and alpha-adrenergic antagonists were also investigated. 2. There were no significant changes in the blood gas values during any of the infusions except for a mean fall in pH of 0.04 during adrenaline infusion. 3. Adrenaline caused a fall in the fetal heart rate followed by a rise above the control value after 15-20 min. The fall in heart rate was abolished when the rise in blood pressure was blocked with phentolamine. The rise in heart rate was blocked by propranolol. The exact cause of the biphasic changes in heart rate during adrenaline infusion is not clear. 4. A fall in heart rate was not seen with noradrenaline; a small rise was. Propranolol changed this into a fall in heart rate while phentolamine increased the size of the heart rate rise. 5. Phentolamine alone increased the fetal heart rate by 25% and reduced blood pressure by 12%; propranolol alone reduced heart rate by 14% and had no effect on blood pressure. Isoprenaline increased fetal heart rate and reduced blood pressure. 6. The incidence of fetal breathing movements was highly variable. Despite this a significant increase was observed during adrenaline infusion. None of the other infusions had consistent effects. 7. The role of the circulating catecholamines in mediating or modifying the cardiovascular responses to hypoxia in the fetal sheep is discussed.
1. Adrenaline and noradrenaline have been infused into the fetal sheep to produce plasma concentrations comparable to those seen during hypoxia. The effects have been compared with those of isoprenaline and methoxamine and the sensitivity to beta- and alpha-adrenergic antagonists has been followed. 2. Adrenaline caused an alpha-mediated increase in blood glucose that is associated with a fall in plasma insulin concentration. It also caused a beta-mediated increase in plasma lactate, free fatty acid and amino acid concentrations. 3. Noradrenaline was much less effective than adrenaline at eliciting metabolic responses. It had not cause a significant change in plasma glucose concentration, although this was associated with a small increase in plasma insulin concentration. It caused a small rise in the concentration of lactate and free fatty acids in fetal plasma but had no effect on plasma amino acids. 4. The beta- and alpha-adrenergic antagonists propranolol and phentolamine alone were without effect on any of the plasma metabolites or hormones assayed. Isoprenaline increased plasma glucose, lactate, free fatty acid, alanine and insulin concentrations, while methoxamine only increased plasma glucose and lactate, and this was associated with a fall in insulin concentration. 5. The concentration of ACTH in fetal plasma was increased by adrenaline and to a lesser extent by noradrenaline and methoxamine; these were blocked by phentolamine. Isoprenaline also caused a small increase in ACTH. There were no corticosteroid changes associated with the increase in ACTH. 6. The results have been discussed in relation to the adrenergic and pancreatic control of metabolism in the fetal sheep.
Synacthen (10 microgram/h) infused into foetal sheep at about day 125 of gestation caused premature delivery within 4 days. During the first 24 h of the infusion the secretion of adrenocorticotrophin was depressed and the assayable hormone concentration was within 500-1000 pg/ml. Subsequently, large fluctuations occurred in the adrenocorticotrophin concentration in the plasma of foetal sheep which were consistent with the stimulation of adrenocorticotrophin secretion. No transfer of Synachthen to non-infused twin foetuses was observed. The plasma corticosteroid concentration in the infused foetus also showed a small rise during the first 24 h of the infusion followed by large fluctuations in concentrations that coincided with the changes in adrenocorticotrophin. No consistent changes in the plasma corticosteroid concentration in the non-infused twin foetus were observed. These results are discussed in relation to the hormone changes occurring during normal delivery.
Synacthen has been infused at 10 microgram/h into 4 hypophysectomized foetal sheep. This caused a rise in adrenocorticotrophin to a mean value of 512 pg/ml which remained fairly constant and did not show the large fluctuations seen on infusion into intact foetuses. The Synacthen half-life in the circulation had a mean value of 0.27 min. Hypophysectomy did not necessarily delay the foetal corticosteroid response to Synacthen infusion. The corticosteroid concentration achieved had a mean value of about 50 ng/ml which is substantially below that for intact foetuses and in one case it was maintained at only 20 ng/ml. Despite this delivery occurred within 5 days. Dexamethasone infusion reduced the plasma adrenocorticotrophin concentration by about 70% and the plasma cortisol concentration by about 60%.
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The effect of repeated increases in plasma ACTH on the production of corticosteroids and androstenedione in the sheep foetus has been investigated. Elevation of foetal plasma ACTH for up to 2 h every 24 h by repeated periods of hypoxia increased the output of cortisol. No consistent effects on foetal or maternal androstenedione concentrations or on maternal oestrogen levels were observed. Repeated short periods of increased foetal plasma ACTH concentration may promote maturation of the foetal adrenal, but there is no increase in androgen secretion by the gland nor is there an increase in oestrogen production by the placenta under such conditions.
The effect of adrenaline on the maternal and foetal plasma ACTH concentration of twelve pregnant sheep with chronically implanted vascular catheters has been studied. Adrenaline infused into the jugular vein of the ewe or foetus produced carotid arterial adrenaline concentrations of 1-9 ng/ml. The foetal plasma ACTH was 253 +/- 73 pg/ml and it showed a fivefold increase during adrenaline infusion; the ACTH concentration achieved was proportional to the plasma adrenaline. In the ewe plasma ACTH was 99 +/- 23 pg/ml. During adrenaline infusion to the ewe this rose by an amount dependent on the adrenaline concentration achieved and there was also a rise in foetal plasma ACTH but no consistent change in foetal plasma adrenaline. There was no reproducible change in plasma corticosteroid concentration during adrenaline infusion into the foetus but a rise in maternal plasma corticosteroid concentration during infusion into the ewes. Because the adrenaline concentrations achieved during the infusions were within the physiological range, the results indicate that circulating catecholamines may directly or indirectly influence the concentration of ACTH in the circulation. Also, physiological rises in plasma catecholamines in pregnant animals may stimulate the release of ACTH from the foetal pituitary.
Catheters were implanted into 16 ewes and their foetuses between days 110 and 124 of gestation. Hypophysectomy was attempted in eight of these foetuses. Continuous infusion of synthetic ACTH (10 microgram/h) or dexamethasone (1mg/24 h) into the foetus, starting between days 124 and 129, induced premature parturition. The concentration of progesterone in the maternal peripheral plasma decreased before parturition in all animals while the level of oestradiol increased in ewes with intact foetuses or in those in which hypophysectomy was incomplete. When hypophysectomy was complete, no increase in the maternal level of oestradiol occurred before delivery. The concentration of 13,14-dihydro-15-oxo-prostaglandin F2alpha increased in the peripheral plasma of ewes with intact or hypophysectomized foetuses infused with ACTH. It is suggested that an intact foetal pituitary gland is required for the rise in the level of oestrogen prepartum, but that this rise is not essential for increased prostaglandin production of parturition.
Periods of spontaneously occurring hypoxia have been observed in fetal sheep. These were associated with increases in the fetal plasma concentration of glucose, lactate, free fatty acids, ACTH and corticosteroids (for a fetus close to term). These changes are similar to those observed during experimentally induced hypoxia. Hypoxia may be a mechanism by which plasma metabolites and ACTH are increased in fetal sheep under physiological conditions, particularly during labour.
The disappearance of 125-I-ACTH from the circulation of 4 pregnant and fetal sheep has been followed after a single injection to the ewe or fetus. The mean metabolic clearance rate for the fetus and the ewe was 55 and 34 ml/min/kg respectively, giving a half-life in each case of about 1 min. The higher fetal than maternal arterial plasma ACTH concentration has been ascribed to a higher rate of secretion rather than a reduced rate of clearance compared with the ewe. There was no evidence of placental transfer of immunologically reactive ACTH.
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