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PubMed1982

Inhibition of aortic chemoreceptor responses by metabolic alkalosis in the cat.

The responses of the same aortic chemoreceptor afferents to steady-state isocapnic hypoxia and to hypercapnia on hyperoxia, before and after the induction of metabolic alkalosis, were investigated in 12 anesthetized cats. Metabolic alkalosis was achieved by intravenous administration of sodium bicarbonate in the average dose of 7 mmol . kg-1. On the average, arterial pH (pHa) increased from 7.383 to 7.650 at an arterial CO2 partial pressure (PaCO2) of 30 Torr. The increase in pHa resulted in a decrease in chemoreceptor activity, the effect being greater at a lower arterial O2 partial pressure. Increases in PaCO2 during hyperoxia resulted in an increased activity of the chemoreceptors both before and after NaHCO3 injection. The stimulatory effect of hypercapnia, however, was attenuated by metabolic alkalosis. At a constant PaCO2, decreases in arterial [H+] by the NaHCO3 administration caused an approximately linear decrease in the chemoreceptor activity. At a constant arterial [H+], higher PaCO2 was associated with a slightly greater activity of the chemoreceptors. These results indicate that the major effect of CO2 is mediated by [H+], but there appears to be another mechanism, albeit small, for the effect of CO2.

Alkalosis↗

PubMed1992

Chemoreceptor and vagal influences on thyroarytenoid muscle activity in awake lambs during hypoxia.

This study was designed to identify the various controllers of thyroarytenoid (TA) activity in lambs during resting breathing, hypocapnic hypoxia, and isocapnic hypoxia. The TA muscle is known as the major adductor of the laryngeal aperture. We assumed that both the chemoreceptors and vagal nerves would interact to inhibit TA activity during hypoxia and to favor the occurrence of hyperpnea as a defense against hypoxia. We recorded TA activity directly in 11 awake lambs, aged 11 to 22 days, and studied them in three groups: four normals, four carotid body denervated, and three vagotomized. To test the contribution of the chemoreceptors to TA activity, we used pure O2 tests (Dejours' test) to silence the effects of the peripheral arterial chemoreceptors on the larynx during resting breathing and during the course of two hypoxia tests (the first: hypocapnic hypoxia; the second: isocapnic hypoxia). Our results confirmed 1) that both the peripheral arterial chemoreceptors and the vagal nerves inhibit the TA activity of 15-day-old lambs, during both resting and hypocapnic hypoxia conditions, and 2) that their effects override the hypocapnic effects that would otherwise recruit the TA muscle and close the glottis during hypocapnic hypoxia. We also found that vagotomy, or the pure O2 test, causes major recruitment of TA activity. These findings confirm that 15-day-old lambs are capable of using sustained hyperventilation as a means of fighting hypoxia, and that, because of the control of both the vagus nerves and the chemoreceptors, the laryngeal dynamic is able to keep the glottis aperture actively open, thereby favoring the hyperpnea.

Animals↗

PubMed1995

Adaptation of carotid chemoreceptors to step increases in PaCO2 in anesthetized cats.

1. The rate of change sensitivity of some carotid chemoreceptors to within-breath changes in PaCO2 would suggest that the half-life of adaptation of these receptors to a step increase is shorter than the 5-10 s previously reported. 2. In six anesthetized cats, step increases in PaCO2 (10 in each cat) were produced by injection of CO2 into the inspired gas during high-frequency jet ventilation. Chemoreceptor discharge was recorded from single-fiber preparations of the divided carotid sinus nerve, and the changes in PaCO2 were followed with the use of an in vivo pH electrode. 3. The adaptation half-lives were 0.3, 0.8, 1.2, 1.3, 1.6, and 8.6 s. The physiological significance of these findings in terms of respiratory control and the mechanism of chemotransduction are discussed. The receptors with the shortest and longest half-lives showed corresponding differences in response to sine-wave oscillations in PaCO2. 4. In a further group of five cats, chemoreceptor responses to step increases in PaCO2 were tested before and during infusion of KCl to produce a mean arterial [K-] of 6.8 +/- 0.2 (SE) mM. Under these conditions the hyperkalemia caused no further increase in discharge. 5. We conclude that adaptation of the chemoreceptor response to increases in PaCO2 is much faster than previously reported and that this finding is consistent with observations of chemoreceptor responses to respiratory PaCO2 oscillations.

Adaptation, Physiological↗

PubMed1994

Role of arterial chemoreceptors in mediating the effects of endogenous adenosine on sympathetic nerve activity.

BACKGROUND: Exogenous adenosine has been shown to increase muscle sympathetic nerve activity (MSNA), blood pressure, heart rate, and ventilation in conscious humans, effects attributed to peripheral chemoreceptor activation. METHODS AND RESULTS: To determine whether endogenous adenosine has similar effects and whether they are mediated through chemoreceptor activation, we examined the effects of dipyridamole, an inhibitor of adenosine reuptake, on sympathetic nerve activity and ventilation. Twenty studies were conducted on separate days in 15 healthy volunteers. We examined responses to dipyridamole 0.56 mg/kg during room air breathing (n = 7), during hyperoxia (100% O2, n = 6), and during room air breathing after pretreatment with aminophylline (n = 7). During room air breathing, dipyridamole increased MSNA from 231 +/- 42 to 504 +/- 136 U/min, heart rate from 65 +/- 3.8 to 96 +/- 4.7 beats per minute, and systolic blood pressure from 129 +/- 3.5 to 140 +/- 4.8 mm Hg; central venous pressure decreased from 5.5 +/- 0.4 to 4.5 +/- 0.3 mm Hg (P < .01), and minute ventilation increased from 7.8 +/- 0.6 to 9.1 +/- 0.5 L/min (P < .01). During peripheral chemoreceptor suppression (with hyperoxia), there was a dissociation of the effects of dipyridamole on ventilation and sympathoexcitation. Effects on ventilation were attenuated, but sympathoexcitatory effects were not. Pretreatment with aminophylline, an adenosine receptor antagonist, either abolished (blood pressure, minute ventilation, and end-tidal CO2) or markedly attenuated (MSNA and heart rate) the effects of dipyridamole during room air breathing. CONCLUSIONS: Augmentation of endogenous adenosine with dipyridamole increases sympathetic nerve activity and ventilation in conscious humans. The ventilatory effects of endogenous adenosine are mediated predominantly by chemoreceptor activation, but the sympathetic and hemodynamic responses to endogenous adenosine are probably mediated by an additional afferent mechanism that is independent of peripheral chemoreceptor activation.

Adenosine↗

PubMed2005

Gene transfer of neuronal nitric oxide synthase to carotid body reverses enhanced chemoreceptor function in heart failure rabbits.

Our previous studies showed that decreased nitric oxide (NO) production enhanced carotid body (CB) chemoreceptor activity in chronic heart failure (CHF) rabbits. In the present study, we investigated the effects of neuronal NO synthase (nNOS) gene transfer on CB chemoreceptor activity in CHF rabbits. The nNOS protein expression and NO production were suppressed in CBs (P<0.05) of CHF rabbits, but were increased 3 days after application of an adenovirus expressing nNOS (Ad.nNOS) to the CB. As a control, nNOS and NO levels in CHF CBs were not affected by Ad.EGFP. Baseline single-fiber discharge during normoxia and the response to hypoxia were enhanced (P<0.05) from CB chemoreceptors in CHF versus sham rabbits. Ad.nNOS decreased the baseline discharge (4.5+/-0.3 versus 7.3+/-0.4 imp/s at 105+/-1.9 mm Hg) and the response to hypoxia (18.3+/-1.2 imp/s versus 35.6+/-1.1 at 40+/-2.1 mm Hg) from CB chemoreceptors in CHF rabbits (Ad.nNOS CB versus contralateral noninfected CB respectively, P<0.05). A specific nNOS inhibitor, S-Methyl-L-thiocitrulline (SMTC), fully inhibited the effect of Ad.nNOS on the enhanced CB activity in CHF rabbits. In addition, nNOS gene transfer to the CBs also significantly blunted the baseline renal sympathetic nerve activity (RSNA) and the response of RSNA to hypoxia in CHF rabbits (P<0.05). These results indicate that decreased endogenous nNOS activity in the CB plays an important role in the enhanced activity of the CB chemoreceptors and peripheral chemoreflex function in CHF rabbits.

Adenoviridae↗

PubMed1980

Responses of the heart to stimulation of aortic body chemoreceptors in dogs.

We stimulated the aortic chemoreceptors in dogs that were anesthetized with chloralose and artificially ventilated by perfusing the isolated aortic arch with venous blood. Inotropic responses were determined by measuring the maximum rate of change of left ventricular pressure (dP/dt max) with aortic pressure and heart rate held constant. Stimulation of the aortic chemoreceptors resulted in an average increase in heart rate of 14 +/- 2.0 beats/min (mean +/- SE) from 166 +/- 7.7 beats/min and an increase in dP/dt max of 501 +/- 85 mm Hg/sec from 3508 +/- 154 mm Hg/sec. These changes were statistically significant (P less than 0.001). The afferent pathway of the reflex was shown to be in the vagus nerves and the efferent pathway in the cardiac sympathetic nerves. In some of the dogs, the carotid chemoreceptors were also stimulated. This resulted in decreases in heart rate and dP/dt max of 48 +/- 24 beats/min and 795 +/- 142 mm Hg/sec. Thus we have shown that stimulation of aortic chemoreceptors evokes chronotropic and inotropic responses opposite to those evoked from stimulation of carotid chemoreceptors.

Animals↗

PubMed1993

Carotid, not aortic, chemoreceptors mediate the fetal cardiovascular response to acute hypoxemia in lambs.

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% N2 and 5% O2 to breathe. The chemoreflex response was measured as decrease in heart rate per decrease in Hb 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.

Animals↗

PubMed1982

Role of peripheral chemoreceptors and central chemosensitivity in the regulation of respiration and circulation.

Adjustments of respiration and circulation in response to alterations in the levels of oxygen, carbon dioxide and hydrogen ions in the body fluids are mediated by two distinct chemoreceptive elements, situated peripherally and centrally. The peripheral arterial chemoreceptors, located in the carotid and aortic bodies, are supplied with sensory fibres coursing in the sinus and aortic nerves, and also receive sympathetic and parasympathetic motor innervations. The carotid receptors, and some aortic receptors, are essential for the immediate ventilatory and arterial pressure increases during acute hypoxic hypoxaemia, and also make an important contribution to respiratory compensation for acute disturbances of acid-base balance. The vascular effects of peripheral chemoreceptor stimulation include coronary vasodilation and vasoconstriction in skeletal muscle and the splanchnic area. The bradycardia and peripheral vasoconstriction during carotid chemoreceptor stimulation can be lessened or reversed by effects arising from a concurrent hyperpnoea. Central chemoreceptive elements respond to changes in the hydrogen ion concentration in the interstitial fluid in the brain, and are chiefly responsible for ventilatory and circulatory adjustments during hypercapnia and chronic disturbances of acid-base balance. The proposal that the neurones responsible for central chemoreception are located superficially in the ventrolateral portion of the medulla oblongata is not universally accepted, mainly because of a lack of convincing morphological and electrophysiological evidence. Central chemosensitive structures can modify peripheral chemoreceptor responses by altering discharges in parasympathetic and sympathetic nerves supplying these receptors, and such modifications could be a factor contributing to ventilatory unresponsiveness in mild hypoxia. Conversely, peripheral chemoreceptor drive can modulate central chemosensitivity during hypercapnia.

Animals↗

PubMed1981

Analysis of inhibitory and excitatory actions of dopamine on chemoreceptor discharges of carotid body of cat in vivo.

Chemoreceptor discharges were recorded from the carotid sinus nerve of the cat in vivo, and their frequency was used as an index of receptor activity. The effects of dopamine on chemoreceptor activity were analyzed in normal and ischemic carotid bodies. Intra-arterial injections of dopamine (DA) induced various patterns of chemoreceptor responses; simple inhibition, inhibition followed by excitation, and simple excitation, depending upon doses and the time interval between two injections. After a large dose of DA, a previous inhibitory response to DA was converted into an excitatory one. Pretreatment of the animal with reserpine (0.1 mg/kg, i.v.) or 5-hydroxydopamine (5 mg/kg, i.v.) also converted the inhibitory response to DA into the excitatory one. After haloperidol (0.1 mg/kg, i.v.), the inhibitory response to DA was completely blocked, and DA induced a dose-dependent increase in chemoreceptor discharges. After 1-hr ischemia of the carotid body, DA induced only the inhibitory response, which was blocked by haloperidol, but did not produce any excitatory responses. Results indicate that DA exerts a self-blocking action on inhibitory dopaminergic receptors which are possibly located on the nerve ending, and that DA, also acting directly on the glomus cell, would produce the chemoreceptor excitation.

Animals↗

PubMed2000

Ventilation- and carotid chemoreceptor discharge-response to hypoxia during induced hypothermia in halothane anesthetized rat.

It has been hypothesized that respiratory "gain" to hypoxic stimulus is not depressed in hypothermic animals though ventilation and that metabolic O(2) demand (Vo(2)) decreases with reduction in body temperature. The present study addressed this hypothesis by quantitative analysis of ventilatory and carotid chemoreceptor responsiveness to hypoxia during induced hypothermia in halothane anesthetized and spontaneously breathing rats. Rectal temperature was lowered from 37 degrees C (normothermia) to 30 and 25 degrees C by cooling body surface at comparable anesthetic depth without inducing shivering. Ventilation (V(E)), V(O2), PaO(2) and carotid chemoreceptor afferent discharges were measured during hyperoxic and hypoxic gas breathing. PaO(2) values at the same Fi(O2) (range 0. 35-0.08) decreased progressively as rectal temperature decreased. Both the V(E)/V(O2)- and chemoreceptor discharge-response curves shifted toward a lower PaO(2) range with a slight increase in the response slopes during hypothermia. The results indicated that the sensitivity of carotid chemoreceptor and ventilatory responses to hypoxia did not decrease at reduced body temperature. It is concluded that carotid chemoreceptor mediated regulation of ventilation is tightly coupled to changes in PaO(2 )range in halothane anesthetized rats during induced hypothermia.

Acid-Base Equilibrium↗

PubMed2003

Influence of the stimulation of central chemoreceptors on the gastric mucosal blood flow in artificially ventilated and spontaneously breathing rats.

Respiratory failure coincides frequently with the occurrence of gastric ulceration. In advanced respiratory insufficiency hypoxemia is often accompanied by hypercapnia, which is the stimulus for central chemoreceptors as well as for carotid body chemoreceptors. The purpose of the work was to investigate the reflex effect of stimulation of central chemoreceptors on gastric mucosal blood flow (GMBF) in the rat. Central chemoreceptors were stimulated by a gas mixture composed of 10% carbon dioxide, 50% oxide and 40% nitrogen. In artificially ventilated and spontaneously breathing animals, the stimulation of central chemoreceptors caused a significant increase in gastric mucosal vascular resistance, accompanied by a marked decline in blood flow. We hypothesize that in patients with respiratory insufficiency accompanied by hypercapnia, the reflex impairment of GMBF may contribute to gastric ulceration.

Administration, Inhalation↗

PubMed1989

Re-setting of the hypoxic sensitivity of aortic chemoreceptors in the new-born lamb.

We tested to see whether the steady-state hypoxic sensitivity of aortic chemoreceptors was re-set during the first 2-3 weeks of post-natal life. Aortic chemo-receptor activity was recorded from the distal end of the cut aortic branch of the cervical vagus in pentobarbitone - anesthetized, new-born lambs. Two groups were studied, the first aged 1-4 days and the second aged 10-19 days. Chemoreceptor discharge increased as hyperbolic function with increasing isocapnic hypoxia in both groups and we quantified the position and the shape of this response curve. It was shifted to the right significantly in the older group of lambs, the mean vertical asymtote increasing from 10.00 to 27.95 torr PO2. No significant difference was found in the horizontal asymotote or in the 'shaping term' between the two groups. The greatest differences between the stimulus-response curves of the two groups of animals with respect to the mean level of discharge and the slope of the curve occurred when PaO2 was below ca. 50 torr. The aortic chemoreceptors of older lambs were unable to maintain a sustained discharge at arterial PO2 values below ca. 30 torr. In contrast, in the younger group PO2 often had to be reduced below this level before discharge increased significantly. We conclude that, like the carotid chemoreceptors, aortic chemoreceptor sensitivity is re-set over the first few weeks of life. The re-setting may contribute to the increase in the ventilatory response to hypoxia which occurs over this period.

Action Potentials↗

PubMed1985

Kidney function during common carotid artery occlusion in anaesthetized cats: influence of vagotomy, constant ventilation, blood pressure stabilization, and carotid body chemoreceptor inactivation.

The reactions of kidney function elicited by bilateral common carotid artery occlusion were studied in six groups of chloralosed cats in which the Nn. vagi, the breathing reaction, the increase of the mean systemic arterial blood pressure, and the carotid body chemoreceptors were excluded successively. Carotid occlusion in the control animals caused a rise of the mean systemic arterial blood pressure, hyperventilation, and an increase in renal sodium and water excretion, resulting from an inhibition of tubular reabsorption. Bilateral cervical vagotomy, relaxation and constant artificial ventilation only slightly modified this renal response. Inactivation of the carotid body chemoreceptors in vagotomized and constantly ventilated cats attenuated the natriuresis due to carotid occlusion regardless of the behaviour of the renal perfusion pressure. On the other hand, keeping the mean arterial blood pressure during carotid occlusion constant by the bleeding technique also reduced the natriuretic reaction. Cats with both inactivated carotid body chemoreceptors and constant renal perfusion pressure exhibited an antinatriuretic reaction during carotid clamping. From these data it is concluded that in narcotized cats the natriuretic response during carotid occlusion is the result of both a stimulation of the carotid body chemoreceptors and the rise of the renal perfusion pressure. In contrast, in dogs this so-called carotid-sinus-polyuria seems to be induced solely by the increase of the systemic arterial blood pressure. The findings additionally indicated that the arterial chemoreceptors may be involved in the physiological daily control of renal sodium excretion already at normal arterial oxygen tension under sea-level conditions.

Anesthesia↗

PubMed1981

Chemoreceptors and their reflexes with special reference to the fetus and newborn.

Such evidence as there is indicates that hypoxia excites peripheral chemoreceptors in the adult by causing a fall in the rate of oxidative phosphorylation and that this process is potentiated by a rise in PCO2 which most probably acts by altering intracellular pH. What is unclear is whether this occurs in Type I cells or in sensory fibres and whether either should be regarded as the primary receptor. There is also uncertainty about the role of noradrenaline and dopamine, which are stored and presumably secreted in the chemoreceptor complex: are they, respectively, excitatory and inhibitory transmitters or do they modulate an underlying chemoreceptive process? In the fetus, the carotid body chemoreceptors are largely insensitive despite an adequate chemical stimulus; they are activated at or shortly after birth by an unknown process and thereafter, in the newborn period, they appear to be involved in sensing chemical changes in arterial plasma and assisting in respiratory stability but there is some evidence that they only become fully effective some days or even weeks after birth. There is now compelling evidence that important if not unique central chemoreceptors, sensitive to changes in pH of brain extracellular fluid are located superficially in the ventro-lateral part of the medulla in the adult but in the fetus it appears that these receptors or their afferent discharge are in some way inhibited such that respiratory activity when it occurs is driven largely by supra-pontine influences, the so-called 'automatic' component of respiratory control being largely if not entirely suppressed. At birth, this component is clearly activated since breathing is continuous and sensitive to chemical stimulation. It is probable that in a proportion of newborn, activation of this component is either imperfect or delayed which would lead to respiratory instability or even failure and this would be more likely to occur in quiet sleep than in rapid-eye-movement sleep or with the newborn awake. A more complete understanding of the changes in sensitivity of the central and peripheral chemoreceptors and their reflexes at birth is required before the reasons for inadequate respiratory control in the newborn period can be appreciated.

Animals↗

PubMed1975

Potencies of doxapram and hypoxia in stimulating carotid-body chemoreceptors and ventilation in anesthetized cats.

The effects of doxapram on carotid chemoreceptor activity and on ventilation (phrenic-nerve activity) were tested before and after denervation of the peripheral chemoreceptors in cats. Doxapram was found to be a potent stimulus to the carotid chemoreceptors; the stimulation produced by 1.0 mg/kg doxapram, iv, equalled that produced by a Pao2 of 38 torr. Doxapram also increased phrenic-nerve activity in doses as low as 0.2 mg/kg, iv. After denervation of the peripheral chemoreceptors, doxapram in doses as large as 6 mg/kg failed to stimulate ventilation. It is concluded that (in anesthetized cats) doxapram in doses of less than 6 mg/kg increases ventilation by direct stimulation of the carotid, and, probably, the aortic, chemoreceptors, not by a direct effect on the medullary respiratory center.

Anesthesia↗

PubMed1980

Effects of substance P on carotid chemoreceptor activity in the cat.

1. The influence of substance P (SP) on spontaneous chemosensory discharge and on responses of the carotid chemoreceptors to various drugs has been investigated in pentobarbitone anaesthetized casts in which chemoreceptor activity was recorded from the peripheral end of a sectioned sinus nerve. 2. After an initial slight inhibition during the first 5--15 sec following the injection, SP (0.1--100 microgram I.A.) caused a dose-related increase in discharge which lasted for 45--300 sec in artificially ventilated cats, discharge being increased by about 50% on average. The increase was of shorter duration when the animals were allowed to breathe spontaneously. 3. The delayed increase in discharge was not secondary to the hypotension caused by SP, nor was it entirely due to changes in bronchomotor tone resulting from direct or indirect actions of SP, although such changes contributed to the response. It was not possible to determine whether the excitation was due to a direct effect of SP on the chemoreceptors. 4. Chemosensory excitation evoked by NaCN (5 microgram I.A.) was potentiated during I.A. infusions of SP and also 10--20 min after SP (10 microgram I.A.) had been injected. In contrast, responses to ACh (50 microgram I.A.) were inhibited. These effects may be due to a nicotinic-blocking action of SP on the carotid chemoreceptors. It was also found that the inhibitory action of dopamine (5 microgram I.A.) was reduced during SP infusion whereas that of 5-HT (10 microgram I.A.) was potentiated. 5. A sample of crude SP had effects on spontaneous chemoreceptor discharge and responses to NaCN and ACh which were qualitatively similar to those obtained using synthetic SP. 6. The physiological significance of the results is discussed and it is concluded that the interpretation depends upon whether or not SP is present in the cat's carotid body.

Acetylcholine↗

PubMed1987

Analysis of cardiovascular responses evoked following changes in peripheral chemoreceptor activity in the rat.

1. Comparisons have been made between rats anaesthetized with pentobarbitone and Saffan (Glaxovet), of respiratory and cardiovascular changes evoked by (1) brief stimulation of carotid body chemoreceptors (c.b.); (2) systemic hypoxia induced by N2 breathing for 5 s; (3) brief unloading of peripheral chemoreceptors with dopamine; and (4) O2 breathing for 10 s. The results are discussed in relation to responses reported in other species. 2. Under pentobarbitone, c.b. stimulation evoked hyperventilation, tachycardia, and vasoconstriction in hindlimb muscle and renal and mesenteric circulation. The effects of vagotomy and/or of holding ventilation constant indicated that the primary cardiac response to c.b. stimulation was bradycardia which could be overcome by tachycardia, due to a reflex mediated by pulmonary stretch receptors with vagal afferents and to other secondary effects of hyperventilation. However, reflex vasodilatation initiated by hyperventilation did not modulate the chemoreceptor-induced peripheral vasoconstriction. 3. Under light pentobarbitone, N2 evoked a similar pattern of response to c.b. stimulation, except that the tachycardia apparently also reflected the known effects of increased central inspiratory drive and central nervous hypoxia on cardiac vagal and sympathetic activity. However, under deep pentobarbitone or after guanethidine, N2 induced generalized vasodilatation. It is proposed that these responses reflected the local vasodilator actions of hypoxia. 4. Under light Saffan anaesthesia, both c.b. stimulation and N2 evoked the autonomic components of the alerting stage of the defence response which includes tachycardia and vasodilatation in hindlimb muscle, which are not secondary to hyperventilation, with renal and mesenteric vasoconstriction, pupillary dilatation and exophthalmus. However, under deep Saffan anaesthesia, c.b. stimulation and N2 produced the patterns of response they each evoked under deep pentobarbitone. It is proposed that light Saffan anaesthesia allows chemoreceptor stimulation to activate the defence areas and that under such conditions the primary response to c.b. stimulation and direct effects of hypoxia may be overridden. 5. Under pentobarbitone or Saffan, the hypoventilation induced by I.V. dopamine and by O2 indicated that almost 50% of eupnoeic ventilation was due to drive from peripheral chemoreceptors. This drive apparently played no significant role in setting the baseline level of heart rate, but could account for 10% of total peripheral resistance and of the baseline level of arterial pressure under Saffan, rather less under pentobarbitone.

Anesthesia, Intravenous↗

PubMed1985

Denervation of peripheral chemoreceptors decreases breathing movements in fetal sheep.

The role of the peripheral chemoreceptors in the control of fetal breathing movements has not been fully defined. To determine whether denervation of the peripheral chemoreceptors affects fetal breathing movements, we studied 14 chronically catheterized fetal sheep from 120 to 138 days of gestation. In seven fetuses the chemoreceptors were denervated by bilateral section of the vagus and carotid sinus nerves; in seven others, sham operations were performed. We compared several variables during two study periods: 0-5 and 6-13 days after operation. In the denervated fetuses there were significant decreases in the incidence and amplitude of fetal breathing movements during both study periods. There were no differences between the two groups in incidence of low-voltage electrocortical activity, arterial pH and blood gas tensions, fetal heart rate, mean arterial blood pressure, or duration of survival after operation or birth weight. We conclude that denervation of the peripheral chemoreceptors decreases fetal breathing movements. These results indicate that the peripheral chemoreceptors are active during fetal life and participate in the control of fetal breathing movements.

Animals↗