Breathing movements in fetal lambs and the effect of hypercapnia.

Chapman, R. A.; Dawes, G. S.; Rurak, D. W.; Wilds, Preston Lea

doi:10.1113/jphysiol.1980.sp013227

Cited by 35 publications

(10 citation statements)

References 12 publications

(17 reference statements)

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“…An alternative, and potentially more interesting, explanation for this inconsistency is that reduced uterine flow and the associated fetal hypoxia may increase rather than reduce the activity in fetal respiratory muscles. In support of this hypercapnia, of the degree observed with the fetal asphyxia reported here, increases fetal breathing (Chapman, Dawes, Rurak & Wilds, 1980) and reduced uterine flow associated with uterine contraction may be associated with enhanced arousal and respiratory activity in the fetal sheep (Harding et at. 1983).…”

Section: Discussionmentioning

confidence: 98%

Metabolic and cardiovascular effects on fetal sheep of sustained reduction of uterine blood flow.

Gu¹,

Jones²,

Parer³

1985

The Journal of Physiology

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SUMMARY1. The effects on the fetus and placenta of graded reductions of uterine blood flow to 30-90 % of control have been studied in sheep at days 125-143 of pregnancy.2. Reduction of uterine flow to 70-90 % of control had little effect upon fetal oxygenation or heart rate or blood pressure but elevated fetal plasma catecholamine concentration.3. Reduction of flow to 30-50 % of control depressed fetal arterial and umbilical venous Po2 but had little effect upon oxygen consumption unless the umbilical venous value fell below about 14 mmHg when it was depressed by up to 30 %. Placental oxygen consumption did not fall and was therefore maintained at the expense of the fetus. Fetal arterial pressure rose by 10-12 mmHg and heart rate fell by about 30 beats/min during the first 10-15 min then rose above its initial value. Plasma adrenaline and noradrenaline concentrations rose progressively at a rate which increased with greater degrees of asphyxia. 4. When uterine blood flow was reduced below one-half of normal, net placental consumption of glucose fell and there was evidence of substantial provision of glucose and lactate from the fetus. Fetal production of lactate increased sharply and much of this appeared to be consumed by the placenta at a rate sufficient to account entirely for the deficit in net glucose consumption. 5. The results are consistent with the hypothesis that the fetus senses even small changes in uterine blood flow that are alone insufficient to elicit significant blood gas changes. When the fall in uterine flow caused by arterial compression is relatively large, nutrient supply to the placenta is maintained at the expense of the fetus and as a result of fetal glucose and lactate production. The elevation of fetal arterial Pco, appears to enhance fetal responses to hypoxia. The results are discussed in relation to the fetal responses to brief and prolonged reductions in uterine blood flow.

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Section: Discussionmentioning

confidence: 98%

Metabolic and cardiovascular effects on fetal sheep of sustained reduction of uterine blood flow.

Gu¹,

Jones²,

Parer³

1985

The Journal of Physiology

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“…Since ethical considerations preclude in utero foetal blood sampling in humans, the present investigators have initiated a comprehensive study of MCP placental transfer in a chronically catheterized pregnant sheep preparation. 17 Preliminary findings indicate that the transfer of MCP across the placenta is rapid (<1 rain.) and that foetal concentrations exceexl maternal at 90 minutes after administration.…”

Section: Tableii Infant Datamentioning

confidence: 90%

Placental transport of metoclopramide: Assessment of maternal and neonatal effects

et al. 1983

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“…the abdomen enlarges and the chest wall is drawn in, both laterally and antero-posteriorly, as shown in sheep using arrays of ultrasound emitters/receivers to measure transit times (Poore & Walker, 1980) or in man as visualized by real-time ultrasound. However, when breathing becomes deeper, as in hypercapnia (Boddy, Dawes, Fisher, Pinter & Robinson, 1974a; Chapman, Dawes, Rurak & Wilds, 1980;Dawes, Gardner, Johnston & Walker, 1982), 1-2 3 the fetal chest becomes stabilized by recruitment of intercostal activity and there is an increase in lateral thoracic width, though the sternum continues to be sucked in. These movements resemble those in human infants delivered prematurely and suffering from the respiratory distress syndrome due to deficiency of pulmonary surfactant.…”

mentioning

confidence: 99%

The central control of fetal breathing and skeletal muscle movements.

Dawes¹

1984

The Journal of Physiology

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106

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Breathing movements in the sheep fetus have been observed from a gestational age of about 40 days. From 95 to 115 days fetal breathing movements are almost continuous, interrupted by apnoea rarely exceeding 2 min. From 115 days until term (about 147 days) breathing and movements of the trunk and limbs are episodic. Breathing normally occurs only during rapid-eye-movement sleep as identified by low-voltage cortical electrical activity. Active movements of the neck muscles occur predominantly in high-voltage electrocortical activity. Hypercapnia or acid cerebrospinal fluid perfusion cause an increase in the regularity and depth of breathing when present, and recruit intercostal and laryngeal abductor activity. Isocapnic hypoxia, however, in contrast to the hyperventilation seen postnatally, causes arrest of fetal breathing movements. This effect is due to a central inhibition. Section of the brain stem, from the caudal hypothalamus rostrally, causes dissociation of fetal breathing movements and electrocortical activity into independent rhythms. Section of the brain stem caudally, in the upper pons or at the inferior colliculus, also causes a dissociation of electrocortical activity from breathing movements, which become almost continuous. Isocapnic hypoxia causes an increase in the rate and depth of breathing movements. It is concluded that the arrest of breathing in intact fetal lambs is not due to a direct effect on the respiratory centre in the medulla. The lumbar polysynaptic flexor reflex response becomes episodic after 115 days gestation but, in contrast to fetal breathing movements, is enhanced during high-voltage electrocortical activity. Isocapnic hypoxia arrests movements of the fetal limbs and trunk and inhibits the lumbar flexor reflex. This inhibition of the reflex is prevented by section of the spinal cord at T12, but persists after section of the brain stem in the upper pons. It is attributed to an action on the medulla, independent of the systemic arterial chemoreceptors. Small doses of pentobarbitone (5 mg/kg) cause arrest of fetal breathing movements by a suprapontine mechanism, abolished by brain stem transection, and inhibition of the lumbar flexor reflex by an action on the spinal cord, persisting after transection at T12. Inhibitors of prostaglandin synthetase (indomethacin, meclofenamate or aspirin) induce continuous fetal breathing movements, while prostaglandin E2 arrests fetal breathing. The site of action is on the medulla, as shown by section of the brain stem and of afferents from the systemic arterial chemoreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)

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Breathing movements in fetal lambs and the effect of hypercapnia.

Cited by 35 publications

References 12 publications

Metabolic and cardiovascular effects on fetal sheep of sustained reduction of uterine blood flow.

Metabolic and cardiovascular effects on fetal sheep of sustained reduction of uterine blood flow.

Placental transport of metoclopramide: Assessment of maternal and neonatal effects

The central control of fetal breathing and skeletal muscle movements.

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