Section Of Carotid Sinus Nerves Research Articles

The impact of acute and chronic catecholamines on respiratory responses to hypoxic stress in the rat

Chronic catecholamine production is associated with desensitisation and down-regulation of adrenergic receptors and occurs in conditions, such as heart failure and myocardial infarction. The effects of further acute adrenergic stimulation, which may occur during exercise, and their subsequent effects on chemosensitivity and ventilation are unclear. Chronic isoprenaline (ISO) increased ventilation by 50% (P < 0.05) yet the sensitivity to graded hypoxia was preserved. Acute noradrenaline (NA) in control animals led to a doubling of ventilation in hyperoxia (P < 0.001), and this difference was preserved in graded hypoxia (P < 0.001). Yet, combination of NA + ISO did not increase ventilation beyond ISO at baseline or in hypoxia. ISO, NA, and NA + ISO all induced a metabolic acidosis (P < 0.05) with enhanced ventilation in partial compensation. Carotid sinus nerve (CSN) section led to a partial loss of catecholamine-induced augmentation in ventilation (P < 0.05), yet direct recording from CSN in vitro suggests catecholamine is inhibitory for CSN discharge. These observations suggest that chronic catecholamine exposure may result in decreased exercise performance as a direct consequence of the hyperpnea to compensate for an increased metabolic rate coupled with acidosis and leading to increased central chemosensitivity. A limited contribution from peripheral chemoreceptors was noted but was not a consequence of catecholamine stimulation of the carotid body.

The carotid body in cardiovascular disease: more chicken and egg than horse and cart?

The carotid body in cardiovascular disease: more chicken and egg than horse and cart?

Cardio-respiratory effects of systemic neurotensin injection are mediated through activation of neurotensin NTS1 receptors

The purpose of our study was to determine the cardio-respiratory pattern exerted by the systemic injection of neurotensin, contribution of neurotensin NTS1 receptors and the neural pathways mediating the responses. The effects of an intravenous injection (i.v.) of neurotensin were investigated in anaesthetized, spontaneously breathing rats in following experimental schemes: (i) control animals before and after midcervical vagotomy; (ii) in three separate subgroups of rats: neurally intact, vagotomized at supranodosal level and initially midcervically vagotomized exposed to section of the carotid sinus nerves (CSNs); (iii) in the intact rats 2 minutes after blockade of neurotensin NTS1 receptors with SR 142948. Intravenous injection of 10μg/kg of neurotensin in the intact rats evoked prompt increase in the respiratory rate followed by a prolonged slowing down coupled with augmented tidal volume. Midcervical vagotomy precluded the effects of neurotensin on the frequency of breathing, while CSNs section reduced the increase in tidal volume. In all the neural states neurotensin caused significant fall in mean arterial blood pressure preceded by prompt hypertensive response. The cardio-respiratory effects of neurotensin were blocked by pre-treatment with NTS1 receptor antagonist. The results of this study showed that neurotensin acting through NTS1 receptors augments the tidal component of the breathing pattern in a large portion via carotid body afferentation whereas the respiratory timing response to neurotensin depends entirely on the intact midcervical vagi. Blood pressure effects evoked by an intravenous neurotensin occur outside vagal and CSNs pathways and might result from activation of the peripheral vascular NTS1 receptors.

Neonatal stress and attenuation of the hypercapnic ventilatory response in adult male rats: the role of carotid chemoreceptors and baroreceptors

Neonatal maternal separation (NMS) is a form of stress that disrupts respiratory control development. Awake adult male rats previously subjected to NMS show a ventilatory response to hypercapnia (HCVR; Fi(CO(2)) = 0.05) 47% lower than controls; however, the underlying mechanisms are unknown. To address this issue, we first tested the hypothesis that carotid bodies contribute to NMS-related attenuation of the HCVR by using carotid sinus nerve section or Fi(O(2)) manipulation to maintain Pa(O(2)) constant (iso-oxic) during hypercapnic hyperpnea. We then determined whether NMS-related augmentation of baroreflex sensitivity contributes to the reduced HCVR in NMS rats. Nitroprusside and phenylephrine injections were used to manipulate arterial blood pressure in both groups of rats. Pups subjected to NMS were separated from their mother 3 h/day from postnatal days 3 to 12. Control rats were undisturbed. At adulthood, rats were anesthetized [urethane (1g/kg) + isoflurane (0.5%)], and diaphragmatic electromyogram (dEMG) was measured under baseline and hypercapnic conditions (Pa(CO(2)): 10 Torr above baseline). The relative minute activity response to hypercapnia of anesthetized NMS rats was 34% lower than controls. Maintaining Pa(O(2)) constant during hypercapnia reversed this phenotype; the HCVR of NMS rats was 45% greater than controls. Although the decrease in breathing frequency during baroreflex activation was greater in NMS rats, the change observed within the range of pressure change observed during hypercapnia was minimal. We conclude that NMS-related changes in carotid body sensitivity to chemical stimuli and/or its central integration is a key mechanism in the attenuation of HCVR by NMS.

Depressive cardio-respiratory effects of somatostatin in anaesthetized rats

Cardio-respiratory effects of intravenous injection of somatostatin were investigated in anaesthetized, spontaneously breathing rats that were: (i) neurally intact and subsequently bilaterally vagotomized in the neck, or (ii) midcervically vagotomized with later vagotomized at the supranodosal level, or (iii) midcervically vagotomized and subjected to section of the carotid sinus nerves (CSNs). Intravenous injection of 100mug/kg of somatostatin before and after midcervical vagotomy-induced immediate slowing down of the respiratory rate and decreased tidal volume, mean arterial blood pressure (MAP) and heart rate. Supranodose vagotomy did not abolish somatostatin-induced respiratory depression. CSNs section eliminated all respiratory effects of somatostatin challenge. In all the neural states, somatostatin caused significant falls in mean arterial blood pressure and heart rate. The results of this study suggest that hypoventilation induced by intravenous somatostatin administration occurs outside vagal afferentation to the medulla and is mediated via carotid body afferents. Sino-aortic chemoreceptors and baroreceptors do not contribute to bradycardia and a fall in blood pressure. These cardiovascular effects are presumably mediated due to excitation of somatostatin receptors within the heart and/or in the brain.

Cyclic phosphatidic acid stimulates respiration without producing vasopressor or tachycardiac effects in rats

The effects of a novel lipid mediator, cyclic phosphatidic acid (cPA), on respiratory and cardiovascular functions were examined in anesthetized rats. Intravenous (i.v.) administration of 3- O-carba-oleoyl-cPA at doses of 130 and 390 μg/kg produced dose-dependent increases in tidal volume and respiratory frequency, resulting in an increase in total ventilation. Heart rate was slightly decreased at a dose of 390 μg/kg, while systemic arterial pressure was not affected. Bilateral section of vagi and carotid sinus nerves designed to eliminate major regulatory inputs from the peripheral afferents to the respiratory center reduced these responses, but did not abolish them. These results indicate that cPA stimulates respiration, via central and peripheral mechanisms acting on the central respiratory rhythm generator in the brain stem. Administration of cPA may be of therapeutic value as a respiratory stimulant without producing vasopressor or tachycardiac effects, for treatment of respiratory disorders.

Carbon dioxide sensitivity during hypoglycaemia‐induced, elevated metabolism in the anaesthetized rat

We have utilized an anaesthetized rat model of insulin-induced hypoglycaemia to test the hypothesis that peripheral chemoreceptor gain is augmented during hypermetabolism. Insulin infusion at 0.4 U kg (-1)min(-1) decreased blood glucose concentration significantly to 3.37 +/- 0.12 mmol l(-1). Whole-body metabolism and basal ventilation were elevated without increase in P(a,CO(2)) (altered non-significantly from the control level, to 37.3 +/- 2.6 mmHg). Chemoreceptor gain, measured either as spontaneous ventilatory airflow sensitivity to P(a,CO(2)) during rebreathing, or by phrenic minute activity responses to altered P(a,CO(2)) induced by varying the level of artificial ventilation, was doubled during the period of hypermetabolism. This stimulatory effect was primarily upon the mean inspiratory flow rate, or phrenic ramp component of breathing and was reduced by 75% following bilateral carotid sinus nerve section. In vitro recordings of single carotid body chemoafferents showed that reducing superfusate glucose concentration from 10 mM to 2 mM reduced CO(2) chemosensitivity significantly from 0.007 +/- 0.002 Hz mmHg(-1) to 0.001 +/- 0.002 Hz mmHg(-1). Taken together, these data suggest that the hyperpnoea observed during hypermetabolism might be mediated by an increase in the CO(2) sensitivity of the carotid body, and this effect is not due to the insulin-induced fall in blood glucose concentration.

Carotid sinus nerve section abolishes NMDA evoked respiratory effects in anaesthetised rats

Respiratory effects of NMDA injection into the right atrium were investigated in 11 urethane-chloralose anaesthetised and spontaneously breathing rats. The animals were initially vagotomised and six of them were subdued to the subsequent carotid sinus nerve section, and the other five were treated by NMDA antagonist. Bolus injection of NMDA (27 micromol/kg) induced the depression of ventilation in all rats, due to the decrease in tidal volume from a baseline of 2.98 +/- 0.4 to 2.63 +/- 0.3 ml (P < 0.01), and slowing down of the respiratory rate from a baseline of 56 +/- 2.6 to 27 +/- 2.0 breaths min(-1) (P < 0.0001). Section of the carotid sinus nerves (CSNs) precluded the respiratory depression. Prolongation of the expiratory time was reduced by this neurotomy from 5.07 +/- 2.6 to 1.04 +/- 0.03 (P < 0.05). In five rats the blockade of NMDA receptors with the selective antagonist (AP-7) was likewise efficient in eliminating the post-NMDA respiratory response. NMDA increased mean arterial blood pressure and this rise occurred beyond the afferentation from the carotid bodies and the blockade of NMDA receptors. Results of this study indicate that inhibition of the respiratory drive evoked by NMDA administered via the peripheral circulation requires intact carotid bodies and activation of NMDA receptors.

Purinergic contribution to circulatory, metabolic, and adrenergic responses to acute hypoxemia in fetal sheep.

This study investigated the effects on femoral vascular resistance, blood glucose and lactate levels, and plasma catecholamine concentrations of fetal treatment with an adenosine receptor antagonist during acute hypoxemia in fetal sheep during late gestation. Under anesthesia, seven fetal sheep were instrumented between 117 and 118 days gestation (term is approximately 145 days) with vascular and amniotic catheters and an ultrasonic probe around a femoral artery. Six days after surgery, all fetuses were randomly subjected to a 3-h experiment consisting of 1 h of normoxia, 1 h of hypoxemia, and 1 h of recovery. This was done during either intravenous infusion of vehicle or the adenosine receptor antagonist [8-(p-sulfophenyl)-theophylline; 8-SPT] dissolved in vehicle. During vehicle infusion, all fetuses responded to hypoxemia with bradycardia, an increase in arterial blood pressure, and femoral vasoconstriction. Increases in blood glucose and lactate concentrations and in plasma epinephrine and norepinephrine concentrations also occurred in all fetuses during hypoxemia. Fetal treatment with 8-SPT markedly attenuated the bradycardic, hypertensive, vasoconstrictor, glycemic, and adrenergic responses to hypoxemia, but it did not affect the increase in blood lactate concentrations during hypoxemia. These data show that adenosine is involved in the mechanisms mediating fetal cardiovascular, metabolic, and adrenergic responses to hypoxemia in fetal sheep. Fetal treatment with 8-SPT mimics the effects of carotid sinus nerve section on fetal cardiovascular function during hypoxemia, suggesting a role for adenosine in mediating fetal cardiovascular chemoreflexes.

Is the aortic depressor nerve involved in arterial chemoreflexes in rats?

Recent anatomical and physiological studies showed that chemoreceptor afferent fibers are present in the rat aortic depressor nerve (ADN), which has been considered to contain exclusively baroreceptor afferent fibers. However, it remains to be proven whether the chemoreceptor afferents of the ADN are practically involved in chemoreflexes. The present study was performed in chloralose/urethane-anesthetized rats of either Sprague–Dawley (SD) or Wistar strain to examine whether the ADN carries sufficient information regarding arterial hypoxia and hypercapnia, and whether the ADN indeed participates in chemoreflexes, the circulatory and respiratory components. It was found in either strain that afferent discharges of the ADN were not affected at all by hypoxia or hypercapnia, whereas those of the carotid sinus nerve (CSN) markedly increased due to these stimuli. Hypoxia produced hypertension, transient bradycardia followed by tachycardia, and respiratory facilitation, which characterize the chemoreflexes. Any of these responses was not affected at all by the ADN section, but all were abolished by the CSN section. Intraaortic injection of cyanide also induced transient bradycardia and respiratory facilitation, but any of them was not affected by the ADN section while all were abolished by the CSN section. Furthermore, electrical stimulation of the ADN produced solely baroreflex responses, i.e. hypotension and respiratory suppression, whereas that of the CSN provoked chemoreflex responses, i.e. early, transient hypertension and respiratory facilitation. In conclusion, the rat ADN does not contain a functionally significant number of chemoreceptor afferent fibers, if at all, and does not appreciably contribute to generation of chemoreflexes.

Catechol activation in rat rostral ventrolateral medulla after systemic isocapnic metabolic acidosis.

The catechol signal recorded using in vivo voltammetry within the rat rostral ventrolateral medulla (RVLM) can be interpreted as a catechol-specific index of the integrated activity of RVLM adrenergic barosensitive bulbospinal and nonbulbospinal neurons. To test the hypothesis that systemic acidosis leads to the activation of RVLM adrenergic neurons, the RVLM catechol signal was observed in rats after mild systemic acidosis (pH 7.20-7.25 for 30 min) induced by 1 M HCl under halothane anesthesia, controlled mechanical ventilation, and continuous infusion of Ringer lactate. Particular attention was paid to ensure that changes in mean arterial pressure (MAP) were <15 mmHg during HCl challenge. Saline administration was not associated with any significant change in all considered variables (n = 5). Mild isocapnic systemic acidosis was associated with an increase in catechol signal (n = 5), irrespective of carotid sinus nerve section (n = 5). In keeping with the aim of the study, there were minor (<15 mmHg) but significant changes in MAP among saline, intact, and deafferented groups. Changes in heart rate were not significant. In conclusion, a catechol activation is observed in the RVLM when arterial pressure is maintained during isocapnic systemic metabolic acidosis. This catechol activation appears primarily centrally mediated. Therefore, adrenergic RVLM neurons may relay inputs from the central respiratory generator to the sympathetic system and/or act as chemosensors for H+ next to the surface of the ventrolateral medulla.

Influence of cervical sympathetic nerves on ventilation and upper airway resistance in the rat.

The cervical sympathetic trunks innervate the carotid bodies, carotid baroreceptors, thyroid gland and the upper airway mucosa, structures which can influence breathing and upper airway resistance. However, their role in the control of ventilation and upper airway patency is poorly understood. A constant airflow was applied to the upper airway through a high-cervical tracheostomy in anaesthetized rats breathing spontaneously through a low-cervical tracheostomy. The peripheral ends of the cut cervical sympathetic trunks were stimulated electrically and airflow resistance and ventilation were measured. The effects of cervical sympathetic trunk section on ventilation were also measured in conscious rats. In conscious rats, cutting the sympathetic trunks caused a decrease in ventilation during normoxia but only slightly affected ventilatory responses to hypoxia and hypercapnia. In anaesthetized rats, sympathetic trunk stimulation caused an inhibition of breathing which was sometimes followed by excitation. These responses were unaffected by alpha- or beta-adrenoceptor blockade but were abolished by cutting the carotid sinus nerves. Sympathetic stimulation also caused a fall in upper airway resistance which was reduced by bypassing the nose, unaffected by propranolol or carotid sinus nerve section and abolished by phentolamine. It was concluded that the cervical sympathetic nerves exert important influences on ventilation and upper airway resistance.

An animal model of the relationship between systemic hypertension and repetitive episodic hypoxia as seen in sleep apnoea.

Multiple factors may be responsible for acute and chronic blood pressure changes during obstructive sleep apnoea. A popular hypothesis is that recurrent episodic hypoxia stimulates chemoreceptors which, in turn, cause sympathetically mediated vasoconstriction and perhaps long-term vascular remodelling. Disruption of sleep architecture secondary to frequent arousals may also cause chronic stress which may contribute to diurnal hypertension. A less likely factor elevating blood pressure is the effect of abrupt intra-thoracic pressure changes on venous return and cardiac output. The rat responds to chronic, recurrent episodic hypocapnic hypoxia (12-s bursts of nitrogen followed by air into Plexiglas chambers, every 30 s, 7 h d-1, 2-4% nadir ambient oxygen) with sustained increase in diurnal blood pressure 11-14 mmHg). Subsequent studies reveal that carotid sinus nerve section (chemodenervation) and chemically induced peripheral sympathetic denervation with the neurotoxin 6-OH dopamine both eliminate this blood pressure-elevating effect of chronic episodic hypoxaemia. Using this model, Sprague-Dawley rats have been challenged with both eucapnic hypoxia and asphyxia and failed to show an additional blood pressure elevation above that caused by hypoxia (hypocapnic) alone. It appears that hypocapnic hypoxia creates a maximal stimulus to the sympathetic nervous system to which the addition of hypercarbia does not increase the blood pressure response. An alternative explanation is that the rat has protective mechanisms that limit the diurnal blood pressure response from further increase.

Carotid sinus nerve section and the increase in plasma cortisol during acute hypoxia in fetal sheep.

1. We studied the effects of acute isocapnic hypoxia on plasma concentrations of adrenocorticotrophic hormone (ACTH) and cortisol in sixteen sheep fetuses at 118-125 days of gestation (term is 147 days). Eight fetuses had their carotid sinus nerves cut (denervation); the remaining eight had these nerves left intact. 2. There were no differences in the plasma concentrations of ACTH or cortisol between intact and denervated fetuses during normoxia. 3. Whilst plasma cortisol increased in early (after 15 min) and late (after 45 min) hypoxia in intact fetuses, the rise in cortisol in denervated fetuses was delayed, increasing significantly only by late hypoxia. 4. In contrast, plasma ACTH concentrations were increased in early and late hypoxia in both intact and denervated fetuses. The rise was smaller in denervated fetuses, but was not significantly different from that in intact fetuses. 5. Our results indicate that, in the sheep fetus, carotid sinus nerve section delays the rise in plasma cortisol in response to acute hypoxia without affecting the ACTH response. Further work is needed to establish the mechanism underlying this effect of denervation.

Regulation of Oxygen Delivery and Consumption in Anesthetized Rats during Acute Hypoxia.

Physiological roles of ventilatory responses to acute hypoxia in the regulation of O2 transport and consumption were evaluated quantitatively in halothane anesthetized and spontaneously breathing rats with or without peripheral chemoreceptor afferents. Ventilation (VE), blood gas values, cardiac output (Q), and whole-body O2 consumption (VO2) were measured at various levels of inspired O2 concentration (FIO2) before and after denervation of carotid chemoreceptor afferents. In the carotid sinus nerve (CSN)-intact rat, the reduction in FIO2 from > 0.27 (hyperoxia) to about 0.10 (mild-moderate hypoxia) elicited an augmentation of VE which was accompanied by a well maintained total amount of O2 delivered to tissue (Q x O2 content of arterial blood, DO2) and VO2. The increase in VE was, however, turned off and the VE value did not differ from that in hyperoxia at FIO2 lower than 0.10 (moderate-severe hypoxia) (hypoxic ventilatory depression, HVD). Significant decreases in Q, DO2, and VO2 were also seen at FIO2 < 0.10. After CSN section, VE, Q, DO2, and VO2 values decreased progressively with the reduction in FIO2 from hyperoxia to mild hypoxia (FIO2 = 0.20-0.15). These findings indicate that the normal DO2 and VO2 are preserved in the presence of carotid chemoreceptor afferents in the FIO2 range > 0.10 and that HVD is accompanied by the decrease in VO2. Summarizing all results, VO2 decreased linearly with the reduction in PaO2 lower than about 60 mmHg or DO2 lower than 4 ml/min/100 g bw (critical PaO2 or DO2 for metabolic suppression), above which VO2 remained unchanged. The decrease in VO2 in lower PaO2 or DO2 levels (hypoxic hypometabolism) ensues perhaps from "adaptive" mechanisms reducing O2 demand when adequate O2 supply to tissue is limited.

The effects of almitrine on (3H)5HT and (125I) endothelin binding to central and peripheral receptors: an in vitro autoradiographic study in the cat.

Recently we have shown that the density of [3H]5HT binding sites in the carotid body (CB) and within the nucleus of the tractus solitarius (NTS) of the cat is increased following unilateral chronic sectioning of the carotid sinus nerve (CSN) (Dashwood et al 1990). [125I]endothelin (ET) binding sites have also been identified in these regions, but these “receptors” are unaffected by CSN section (Spyer et al 1991). There is physiological evidence that both 5HT (Kirby and McQueen 1984) and ET (Spyer et al 1991) affect chemoreflex activity in the cat. Here we report the effect of chronic chemoreceptor stimulation, by almitrine bismesylate, on the density of central and peripheral 5HT and ET receptors in the cat.KeywordsCarotid BodyGlomus CellNodose GanglionCarotid Sinus NerveCentral Cardiovascular ControlThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Release of dopamine from carotid sinus nerve fibers innervating type I cells in the cat carotid body.

This study presents evidence that dopaminergic neurons innervate the cat carotid body. Immunocytochemical studies revealed many tyrosine hydroxylase (TH)-positive nerve fibers in the carotid body which establish extensive contacts with type I cells. All TH-positive intralobular profiles disappeared with chronic carotid sinus nerve (CSN) section, but survived sympathectomy following removal of the superior cervical ganglion. The level of endogenous dopamine (DA) in the CSN was higher than that for norepinephrine (NE). While both catecholamines were synthesized by the nerve at similar rates, NE synthesis was abolished by chronic sympathectomy, but DA synthesis remained largely unchanged following this procedure. Our data indicate that DA is not present in the CSN as a mere precursor of NE. Following a 3-hour incubation of carotid bodies with their attached nerves in media containing 20 microM 3H-tyrosine, electrical stimulation of CSN C-fibers in chronically sympathectomized preparations provoked the release of 3H-DA, but not 3H-NE.

Delayed poststimulus decrease of phrenic motoneuron output produced by phrenic nerve afferent stimulation.

The immediate effects of phrenic afferent nerve activation on ventilation have been shown to be both excitatory and inhibitory. Long-lasting inhibitory effects on respiratory motoneuron output have been reported after stimulation of afferent nerves from limb muscles. However, whether respiratory muscle afferent nerves can produce this effect is unknown. We therefore hypothesized that activation of phrenic afferent nerves may produce a prolonged decrease of respiratory motoneuron output. Six alpha-chloralose-anesthetized dogs were studied after vagotomy and bilateral carotid sinus nerve section. The dogs were paralyzed, and end-tidal CO2 was controlled by mechanical ventilation. The proximal end of the cut thoracic phrenic nerve was electrically stimulated for 1 min at intensities that produced activation of thin-fiber afferents. The contralateral efferent phrenic integrated electroneurogram (ENG) was recorded. During stimulation, phrenic ENG activity increased. ENG activity was recorded during recovery and reached a peak decrease compared with control of 19 +/- 11% (SD) 9.0 +/- 6 min after stimulation and returned to control after 30 min. A qualitatively similar response was seen after stimulation of the gastrocnemius nerve. We conclude that activation of thin-fiber afferents in the phrenic nerve can produce a delayed and prolonged decrease of respiratory motoneuron output similar to that of limb muscle afferent nerves.

Role of the rostral ventrolateral medulla in the generation of synchronized sympathetic rhythmicities in the rat

In artificially ventilated, paralyzed rats anesthetized with Nembutal or urethane, power density spectral analysis (PDS), using direct FFT algorithm, was used to quantify rhythmicities in the sympathetic cervical and lumbar nerves after bilateral microinjections into rostral ventrolateral medulla (RVLM) of CoCl 2 and MgCl 2—unspecific synaptic transmission blockers. Later overall sympathetic activity, phrenic nerve discharge, heart rate and arterial blood pressure were recorded. Block of synaptic transmission in RVLM was tested by elimination of sympathoinhibitory or sympathoexcitatory reflex responses to aortic nerve and vagal afferents stimulation respectively. In animals vagotomized with bilateral section of carotid sinus nerve the power in all frequency bands was very significantly reduced to a level not different from that which remained after spinal cord transsection. If carotid baroreceptors were intact, a small peak corresponding to cardiac frequency band persisted. Overall, non-synchronized sympathetic activity and arterial blood pressure increased. All effects were transient, lasted up to 15 min, and could be reproduced several times in one experiment. Respiratory rhythmic activity was unchanged yet respiratory-sympathetic synchronization was abolished. It is concluded that RVLM reticulospinal sympathoexcitatory neurons are responsible for non-synchronized tonic sympathetic activity but are not able to generate synchronized sympathetic rhythms. Synaptic input, presumably inhibitory, either from local neuronal circuits within ventral medulla and/or from other brain stem neuronal circuities is needed to shape out the flexible pattern of sympathetic oscillations.

Reflex control of fetal arterial pressure and hormonal responses to slow hemorrhage

Late-gestation fetal sheep respond to slow hemorrhage with increases in plasma concentrations of adrenocorticotropic hormone (ACTH), hydrocortisone, arginine vasopressin (AVP), and plasma renin activity (PRA) that correlate to the acidemia and hypercapnia also produced by hemorrhage. This study was designed to investigate the role of peripheral chemoreceptors in the mediation of these responses. Chronically catheterized fetal sheep were left intact or were subjected to bilateral section of cervical vagosympathetic trunks and carotid sinus nerves. At least 5 days after surgical preparation (between 121 and 138 days of gestation) fetuses were bled at a rate of 11 ml/10 min for 2 h. Denervated fetuses were studied with or without simultaneous infusion of phenylephrine. Denervation exaggerated the decrease in mean arterial pressure and arterial pH and the increase in arterial PCO2 during hemorrhage. Infusion of phenylephrine in the denervated fetuses prevented the decrease in blood pressure and reduced the magnitudes of changes in blood gases. Fetal plasma ACTH, hydrocortisone, and PRA responses to the hemorrhage were exaggerated in the denervated fetuses (not infused with phenylephrine) compared with the intact fetuses. Phenylephrine infusion attenuated the ACTH response and inhibited the AVP response but did not alter the PRA response. We conclude that the sectioned fibers are important for the maintenance of blood pressure and blood gases during hemorrhage and that the PRA, AVP, and ACTH responses to slow hemorrhage are not mediated by peripheral chemoreceptors.