Hypoxaemia and aortic chemoreceptor function in foetal lambs

Dawes, G. S.; Duncan, Sheila L. B.; Lewis, B. V.; Merlet, C; Owen-Thomas, J.B.; Reeves, J. T.

doi:10.1113/jphysiol.1969.sp008745

Cited by 88 publications

(39 citation statements)

References 7 publications

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“…In contrast to our results, Dawes et al (7) suggested that the response to acute hypoxemia is mediated entirely by the aortic and not by the carotid chemoreceptors. However, the fetal lambs they studied were hyperoxemic instead of normoxemic; their baseline arterial Po2 was 37.8 +.…”

Section: Discussioncontrasting

confidence: 56%

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Carotid, Not Aortic, Chemoreceptors Mediate the Fetal Cardiovascular Response to Acute Hypoxemia in Lambs

Bartelds

et al. 1993

Pediatr Res

102

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ABSTRACI'. The fetal cardiovascular response to acute hypoxemia consists of a decrease in heart rate, a variable change in mean arterial pressure, and an increase in peripheral vascular resistance. This response is mediated by the arterial chemoreceptors. To determine whether chemoreceptors in the carotid artery or in the aorta mediate the fetal cardiovascular response to acute hypoxemia, we studied the response to acute hypoxemia in fetal lambs at 125 to 130 d of gestation after selective carotid (six fetuses) or aortic (five fetuses) denervation. One to 3 d after insertion of catheters, hypoxemia was induced by inflating a balloon occluder around the ewe's hypogastric artery or by giving the ewe 95% Nz and 5% 0 2 to breathe. The chemoreflex response was measured as decrease in heart rate per decrease in H b O2 saturation. To validate our results, we also studied the response to chemical stimulation of the chemoreceptors by injection of sodium cyanide into the inferior vena cava. We found that carotid denervation abolished the heart rate and peripheral vascular resistance responses to hypoxemia but that aortic denervation did not. Responses after injection of sodium cyanide were similar.to those seen during acute hypoxemia. We conclude that the carotid chemoreceptors, and not the aortic chemoreceptors, mediate the fetal cardiovascular response to acute hypoxemia. (Pediatr Res 34: [51][52][53][54][55] 1993) Abbreviations AHRIASa02, decrease in heart rate to decrease in oxygen saturation AHRIABP, decrease in heart rate to increase in mean arterial pressure NaCN, sodium cyanideThe fetal cardiovascular response to acute hypoxemia consists of a decrease in heart rate, a variable change in mean arterial pressure, an increase in peripheral vascular resistance, and a redistribution of blood flow (1-3). The changes in heart rate are mediated by arterial chemoreceptors located in the common carotid artery and aortic arch (4-6). Changes in arterial pressure, peripheral vascular resistance, and blood flow redistribution are mediated in part by chemoreceptors, but also by local mechanisms (3). However, whether the carotid or the aortic chemore- Based on studies in fetal lambs, Dawes et al. (7) suggested that the aortic chemoreceptors mediate the response to acute hypoxemia. They also suggested that the carotid chemoreceptors are inactive in the fetal physiologic range (8), although carotid-nerve activity has been recorded in fetal lambs (9). However, all of these experiments were performed in acutely exteriorized fetal lambs, whereas the ewe was given chloralose anesthesia. The effects of exteriorization and anesthesia may have influenced the results.The aim of this study was to determine whether chemoreceptors located in the carotid artery or in the aorta mediate the fetal cardiovascular response to acute hypoxemia. To avoid any effects of exteriorization and anesthesia, we studied the response to hypoxemia in six carotid-and five aortic-chemoreceptor-denervated fetal lambs chronically instrumented in urero at 125 to 13...

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Section: Discussioncontrasting

confidence: 56%

“…Based on studies in fetal lambs, Dawes et al (7) suggested that the aortic chemoreceptors mediate the response to acute hypoxemia. They also suggested that the carotid chemoreceptors are inactive in the fetal physiologic range (8), although carotid-nerve activity has been recorded in fetal lambs (9).…”

mentioning

confidence: 99%

Carotid, Not Aortic, Chemoreceptors Mediate the Fetal Cardiovascular Response to Acute Hypoxemia in Lambs

Bartelds

et al. 1993

Pediatr Res

102

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“…The fact that vagotomy abolished the initial bradyeardia seen during hypoxia could then be due to interruption of either afferent or efferent fibres, and firm conclusions cannot be drawn from it. Dawes et al (1969) reported that the bradycardia was dependent on afferents from the aortic bodies rather than other vagal afferents because changes in heart rate were depressed purely by cutting the aortic nerves. This is a valid conclusion from their study.…”

Section: Heart Ratementioning

confidence: 99%

Afferent and efferent components of the cardiovascular reflex responses to acute hypoxia in term fetal sheep.

Giussani¹,

Spencer²,

Moore³

et al. 1993

The Journal of Physiology

305

413

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SUMMARY1. We studied the effects of acute isocapnic hypoxia on arterial and central venous pressures, carotid and femoral blood flows and heart rate in intact and carotid denervated fetal sheep between 118 and 125 days gestation, after pre-treatment with either saline, atropine or phentolamine. Electrocortical activity (ECoG) and the incidence of fetal breathing movements (FBM) were also compared between intact and carotid denervated fetuses.2. There were no significant differences between intact and denervated fetuses in any variable measured during normoxia. Soon after the onset of hypoxia a marked bradyeardia occurred in intact, but not in denervated fetuses. Femoral blood flow and femoral vascular resistance (perfusion pressure/femoral blood flow) increased in intact, but not in denervated fetuses. Carotid blood flow increased in both groups of fetuses during hypoxia, but carotid vascular resistance did not change. During hypoxia, the incidence of FBM and low-voltage ECoG was similarly reduced in both groups of fetuses.3. Atropine produced a rise in fetal heart rate during the control period in intact but not in denervated fetuses. At the onset of hypoxia atropine prevented the initial bradycardia seen in intact fetuses. In denervated fetuses a further increase in heart rate occurred throughout the hypoxia.4. All denervated fetuses treated with phentolamine died during the hypoxic challenge, but nine out of fourteen intact fetuses treated with phentolamine survived.5. In intact fetuses which survived hypoxia after treatment with phentolamine, the increase in arterial blood pressure was smaller and the increase in femoral resistance did not occur. In these fetuses a rise in heart rate occurred in hypoxia. Carotid vascular resistance decreased during hypoxia after administration of phentolamine.6. Our results indicate that the initial cardiovascular responses of the late gestation sheep fetus to hypoxia are reflex, and that the carotid chemoreceptors provide the afferent limb of this reflex. The bradyeardia is mediated through a muscarinic pathway, as it is blocked by atropine. The femoral vasoconstriction is MS 9935 D. A. GIUSSANI AND OTHERS mediated through an ac-adrenergic mechanism, mediated both neurally by a carotid chemoreflex and via catecholamines released directly from the adrenal medulla. Both these components are blocked by phentolamine.7. The differences in survival between intact and denervated fetuses during hypoxia after phentolamine suggest that the carotid chemoreflex response to hypoxia involves mechanisms in addition to vagal efferents to the heart and a-adrenergic actions at peripheral blood vessels. These additional mechanisms are as yet undefined, but clearly play an important role in fetal survival during acute episodes of hypoxia.

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“…However they did not specify the criteria used for recognizing chemoreceptor activity, nor the intensity of the hypoxia. Dawes and co-workers (Dawes, Lewis, Milligan, Roach & Talner, 1968; Dawes, Duncan, Lewis, Merlet, Owen-Thomas & Reeves, 1969a) found that reflex changes in blood pressure or in hind limb vascular resistance could be evoked in fetal lambs from 90 days onwards by causing Pa, 0 to fall from about 40 mmHg to about 20 mmHg, or by injecting NaCN into the left atrium. They concluded that the reflexes involved the aortic chemoreceptors since they were abolished by section of the vagi or aortic nerves, whilst section of the carotid sinus nerves had no effect, or even potentiated the response.…”

Section: Introductionmentioning

confidence: 99%

The response to hypoxia of arterial chemoreceptors in fetal sheep and new‐born lambs.

Blanco¹,

Dawes²,

Hanson³

et al. 1984

The Journal of Physiology

261

133

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SUMMARY1. Carotid chemoreceptor activity was detected in each of fourteen halothane or pentobarbitone anaesthetized exteriorized fetal lambs of 90-143 days gestational age.Activity was about 5 Hz at a Pa°, of 25 mmHg and it increased as Pa°2 was reduced, either by compressing the umbilical cord or by reducing the (Flo2) oxygen fraction of the gas used to ventilate the ewe.2. Activity increased briskly when 1-2 ml CO2-saturated saline was injected retrogradely into the lingual artery, but not when saline of pH 7'4 or fetal arterial blood was injected.3. In two fetuses near-term chemoreceptor activity was recorded continuously whilst the umbilical cord was ligated and ventilation with air started. Activity increased 200-500 % as Pa°2 fell, but then fell to below control as Pa,°r ose. We suggest that these changes in activity reflect those occurring naturally at birth.4. No spontaneous chemoreceptor activity could be detected on the day of birth in twelve pentobarbitone anaesthetized lambs delivered vaginally or by Caesarean section at 135-146 days. Single baroreceptor activity could however be recorded in these lambs, and chemoreceptor activity could be elicited by hypercapnia. Spontaneous chemoreceptor activity was detected in six of seven lambs more than 2 days old.5. In eight conscious lambs the steady-state respiratory response to isocapnic hypoxia was variable on the day of birth. In six of these lambs the response was significantly greater by the third day.6. We conclude that the arterial chemoreceptors are active and responsive in the fetus, but quiescent in the lamb on the day of birth when Pa 02 has risen. The hypoxic sensitivity of the chemoreceptors is reset from the fetal to the adult range over the next few days.

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Hypoxaemia and aortic chemoreceptor function in foetal lambs

Cited by 88 publications

References 7 publications

Carotid, Not Aortic, Chemoreceptors Mediate the Fetal Cardiovascular Response to Acute Hypoxemia in Lambs

Carotid, Not Aortic, Chemoreceptors Mediate the Fetal Cardiovascular Response to Acute Hypoxemia in Lambs

Afferent and efferent components of the cardiovascular reflex responses to acute hypoxia in term fetal sheep.

The response to hypoxia of arterial chemoreceptors in fetal sheep and new‐born lambs.

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