Cervical Sympathetic Activity Research Articles

Chronic intermittent hypoxia increases sympathetic responsiveness to hypoxia and hypercapnia

We sought to determine whether chronic exposure to intermittent hypoxia (CIH) increases sympathetic responsiveness to subsequent chemoreflex stimulation. Sprague-Dawley rats were exposed to 30 days of CIH: exposure chamber %O2 [fractional concentration of chamber O2 (FcO2)] nadir 6.5-7% with return to 21% each minute for 8 h/day during the diurnal sleep period (Exp group). Sham controls (SC group) were similarly handled but kept at 21% FcO2 and compared with unhandled controls (UC group). Rats were then anesthetized with urethan, and preganglionic cervical sympathetic activity (CSA), diaphragm electromyogram, arterial pressure, and electrocardiogram were recorded while the rats were spontaneously breathing 100% O2, room air, 10% O2, 12% CO2, and 10% O2-12% CO2. CSA and heart rate were also recorded during phenylephrine infusion to assess baroreceptor function. Mean arterial pressure was significantly greater in Exp than in SC and UC rats during all conditions (P < 0. 05). A vasopressor response to 10% O2-12% CO2 was observed only in Exp rats. CSA was greater in Exp than in SC and UC rats during 10% O2, 12% CO2, and 10% O2-12% CO2 but not during room-air exposure. A significant increase in CSA compared with room air was noted during 10% O2, 12% CO2, and 10% O2-12% CO2 in Exp but not in SC or UC rats. No differences in baroreceptor function were observed among groups. We conclude that CIH leads to increased sympathetic responsiveness to chemoreflex stimulation.

Effect of cervical sympathectomy and hypoxia on the heterogeneity of O2 saturation of small cerebrocortical veins.

This study evaluated the hypothesis that the sympathetic nervous system was one of the factors increasing the heterogeneity of cerebrocortical venous O2 saturation and this heterogeneity would be greater during hypoxia when cervical sympathetic activity was elevated. Thirty-two male Long-Evans rats were either sham operated (n = 16) or received bilateral cervical sympathectomy (n = 16). One-half of the animals (n = 8) in each treatment were challenged by hypoxia (8% O2 in N2). Cerebral blood flow was determined in five brain regions with [14C]iodoantipyrine. Oxygen saturation was measured microspectrophotometrically in small cerebrocortical arteries and veins. The degree of hypoxic hyperemia was not significantly different between sham-operated and sympathectomized rats. Cortical venous O2 saturations, indicating the balance between O2 supply and consumption, were significantly more heterogeneous in the sham-operated group under both normoxic and hypoxic conditions. The coefficient of variation (CV = 100 x SD/mean) for the normoxic sham-operated animals was 24.9% and the average venous O2 saturation was 53.8%. During hypoxia, venous O2 saturation was significantly decreased to 43.1% without a change in CV (24.5%). Sympathectomy significantly reduced this heterogeneity through a reduction in the number of low O2 saturation veins (CV = 13.2%) under normoxic conditions and the effect was similar under hypoxic conditions (CV = 15.3%). In both sham-operated and sympathectomized groups, hypoxia elicited a significantly higher cerebrocortical O2 consumption. Thus, bilateral cervical sympathectomy improved the O2 supply in selective cerebrocortical regions with high O2 extraction. However, the effect of sympathetic innervation on the heterogeneity of cerebrocortical venous O2 saturation was not potentiated by hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Central respiratory modulation of subretrofacial bulbospinal neurones in the cat.

1. Spontaneous activity was recorded from spinally projecting neurones of the subretrofacial nucleus (s.r.f.) in seven chloralose-anaesthetized, vagotomized, paralysed cats. Nineteen such neurones were identified by their antidromic response to stimulation of the ipsilateral dorsolateral funiculus at C5: their axonal conduction velocities were between 2.1 and 9.1 m/s (mean 5.4), and all were silenced by raising the pressure in the ipsilateral carotid sinus (prepared as a blind sac) to 200 mmHg. DL-homocysteic acid was applied ionophoretically to six of these cells, and these were all excited. 2. Activity was recorded simultaneously from the right phrenic nerve and left cervical sympathetic trunk. The phrenic neurogram was taken as an index of central respiratory drive and used to trigger histograms of s.r.f. neurone activity within the respiratory cycle. To eliminate indirect effects via pressure fluctuations, the remaining arterial baroreceptors were disabled during tests by deflation of the ipsilateral carotid sinus and either section of the contralateral sinus nerve (six cats) or occlusion of the carotid artery (one cat). Phrenic-triggered averages of cervical sympathetic activity were also constructed for comparison. 3. Respiratory modulation was detected in the activity of sixteen out of nineteen s.r.f. neurones. Twelve showed an inspiratory peak in activity that was superimposed on a steady discharge maintained throughout the cycle. Five of this group additionally displayed a post-inspiratory dip in activity to below the late expiratory level, and this feature was also seen in one further cell without any detectable inspiratory peak. Three neurones showed an inverse pattern, with reduced or no activity during inspiration, followed by a 'rebound' increased activity level during the post-inspiratory period. The remaining three cells had no discernible respiratory rhythm. 4. Raising end-tidal CO2 levels increased the degree of respiratory modulation in all six inspiratory-firing cells tested as well as one cell showing inspiratory inhibition. Within the range tested, CO2 had no clear effect on the respiratory modulation of two other cells showing inspiratory inhibition and one showing only post-inspiratory depression. No consistent relation was apparent between the overall firing rate of neurones and end-tidal CO2. 5. These results are discussed with reference to the respiratory modulation of sympathetic neurone activity. It is suggested that s.r.f. neurones supply respiratory-related as well as tonic drive to preganglionic neurones.

Ventral medullary surface inputs to cervical sympathetic respiratory oscillations

To examine the effects of focally cooling three areas (rostral, intermediate, and caudal) of the ventral medullary surface (VMS) on respiratory oscillations in cervical sympathetic and phrenic nerve activity, 12 cats were anesthetized, vagotomized, paralyzed, and artificially ventilated with 7% CO2 in O2. Cooling the intermediate area from 37 to 20 degrees C significantly reduced the magnitude of respiratory oscillations in both cervical sympathetic activity (P less than 0.001) and phrenic activity (P less than 0.001). Graded cooling of all three areas caused graded reductions in sympathetic respiratory-related activity that were comparable to the reductions in phrenic activity. The magnitude of the reductions in sympathetic respiratory oscillations was greatest for the intermediate area, followed in order by the caudal and rostral areas. Eight cats also underwent graded VMS cooling while ventilated with 3% CO2 in O2 and 100% O2. At each level of inspired CO2, graded cooling resulted in graded reductions in respiratory oscillations in sympathetic activity; conversely, at each medullary temperature, graded increases in inspired CO2 caused graded increases in cervical sympathetic respiratory activity. These results suggest that all three areas of the VMS influence respiratory oscillations in cervical sympathetic activity, although to different extents.

Effect of focal cooling of central chemosensitive areas on cerebral ischemic response.

The ventrolateral medullary surface (VMS) has been shown to have chemosensitive areas that can alter blood pressure and respiration. It has also been shown that lesions near the VMS can affect the intensity of the cerebral ischemic response (CIR). To determine which regions of the central chemosensitive areas of the ventral medullary surface contribute to the pressor response caused by cerebral ischemia, we used focal cooling of the caudal Loescheke's (CL), intermediate Schlaefke's (IS), and rostral Mitchell's (RM) areas of VMS during ischemia of the brain. Experiments were performed on 17 pentobarbital sodium-anesthetized, paralyzed, and artificially ventilated cats after denervation of the vagi and sinoaortic nerves. Bilateral occlusion of the external carotid and vertebral arteries resulted in a significant increase of arterial pressure (from 129 +/- 4 to 174 +/- 8 mmHg, P less than 0.01) and an increase in splanchnic sympathetic activity. However, heart rate and cervical sympathetic activities were not appreciably affected by cerebral ischemia. Bilateral cooling of the IS area to as low as 10 degrees C led to a decrease or disappearance of phrenic activity but failed to affect the magnitude of the pressor response. Also cooling of the CL and RM areas and application of Gelfoam pledgets soaked in lidocaine (4%) to these areas did not affect the CIR. However, covering the whole VMS with 0.2 ml of 4% lidocaine or cold cerebrospinal fluid (10 degrees C) abolished the ischemic reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Association between sympathetic nerve activity and cerebrovascular protection in young spontaneously hypertensive rats.

The purpose of this study was to determine resting and maximal superior cervical sympathetic nerve activity in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) at five and ten weeks of age as hypertension was developing. Basal cervical sympathetic nerve activity (SNA) of five week SHR was 58 +/- 3 muv* which was significantly elevated over age-matched WKY (SNA = 30 +/- 4 muv, *p less than 0.001) and ten week SHR (SNA = 30 +/- 4 muv, *p less than 0.001) as well as ten week WKY (SNA = 24 +/- 4 muv, *p less than 0.001). Thus, during basal conditions five week SHR nerve traffic was approximately two times that found in age-matched WKY as well as in ten week SHR and WKY. The peak sympathetic nerve activity in response to rapid hemorrhage in five week SHR (215 +/- 16 muv*) was significantly elevated over the maximal response of WKY (140 +/- 23 muv) (*p less than 0.02). Ten week SHR also reached a maximal sympathetic nerve activity (187 +/- 28 muv*) that was significantly elevated over WKY (100 +/- 15 muv) (*p less than 0.02). Thus, both five and ten week SHR had a greater capacity for elevated nerve activity following rapid hemorrhage than age-matched WKY. The elevation in resting cervical sympathetic activity in five week SHR, and the elevated capacity for sympathetic neural response in both five as well as ten week SHR, are consistent with a central nervous system abnormality in SHR that could relate to the previously described protective influence of sympathetic nerves on SHR cerebral blood vessels as hypertension is developing.

The effects of etomidate on arterial pressure, pulse rate and preganglionic sympathetic activity in cats.

We have studied the effects of etomidate on preganglionic cervical sympathetic activity, arterial pressure, and pulse rate. Normal and baroreceptor-denervated animals were studied. On the basis of findings it is concluded that etomidate exerts a minimal direct depressant action on the cardiovascular system. A profound depression of sympathetic tone was observed in spite of unaffected arterial pressure. Etomidate was also shown to possess a mild vagolytic action.

CENTRAL SYMPATHETIC DISCHARGE AND MEAN ARTERIAL PRESSURE DURING HALOTHANE ANAESTHESIA

SUMMARY The effects of halothane on preganglionic cervical sympathetic activity and arterial pressure have been measured in intact and spinal cats, one dog and one baboon. The typical response was an early increase in sympathetic discharge as arterial pressure began to fall. Thereafter, although sympathetic activity declined progressively, at the time it regained the control level arterial pressure was already substantially reduced. At mean arterial pressures of 30–40 mm Hg pronounced increases in sympathetic activity occurred with little change in arterial pressure. Substitution of 70 per cent nitrous oxide for nitrogen during halothane administration usually increased the discharge rate. When halothane was discontinued, recovery of sympathetic discharge was slower than that of arterial pressure. In spinal cats, halothane significantly depressed preganglionic activity.

Aktivitätsänderungen im cervikalen Sympathikus während spinaler Hypothermie

In lightly anesthetized cats immobilized with succinyl choline, sympathetic activity was recorded from filaments of the cervical sympathetic chain during selective cooling of the spinal cord. Spinal cord cooling increased, as a rule, cervical sympathetic activity. During the single periods of experimentation the degree of this activation seemed to be independent of the degree of spinal cord hypothermia. The changes of systemic circulation accompanying this cold-induced sympathetic activation were only slight and inconsistent. This has already been shown in dogs with intact proprioceptive circulatory control. The possible mechanisms by which this constancy of systemic circulation is achieved are discussed.

Factors affecting the cat carotid chemoreceptor and cervical sympathetic activity with special reference to passive hind-limb movements.

1. Recordings have been made of the activity in carotid body chemoreceptor afferent fibres and in the cervical sympathetic of the cat during passive movement of the hind limbs.2. The chemoreceptor activity increases immediately the limbs are moved and is maintained at a raised level with preservation of the chemoreceptor rhythm fluctuations throughout. In some cases, the increase persists for a time after the movements are stopped.3. This early change does not occur if the cervical sympathetic on the same side as the carotid body from which recordings are made is cut, nor does it occur if the femoral and sciatic nerves are cut.4. The carotid artery oxygen tension (P(a, O2)) increases early; in the majority of experiments, there was no significant change in end-tidal P(CO2) although the minute volume of ventilation (V) increased by about 20% of control with passive movement of the hind limbs.5. Passive movement of the hind limbs also causes an immediate rise in cervical sympathetic activity which is sustained, and which is abolished if the femoral and sciatic nerves are cut.6. Electrical stimulation of the cervical sympathetic causes an increase in chemoreceptor afferent discharge.7. Bilateral cervical sympathectomy causes the respiratory lag to increase from approximately 1 sec to some 20 sec and, when passive movements cease, the fall in V is more sluggish than control.8. These results are discussed in the light of the controversy regarding humoral and neurogenic causes for the increase in respiration in exercise.