Suppression of inferior alveolar nerve-induced vasoconstrictor response by ongoing cervical sympathetic nerve activity in cat

This study was designed to evaluate the importance of sympathoadrenal activation in the acute cardiovascular response to apneas and the role of hypoxemia in this response. In addition, we evaluated the contribution of the vagus nerve to apnea responses after chemical sympathectomy. In six pigs preinstrumented with an electromagnetic flow probe and five nonpreinstrumented pigs, effects of periodic nonobstructive apneas were tested under the following six conditions: room air breathing, 100% O2 supplementation, both repeated after administration of hexamethonium (Hex), and both repeated again after bilateral vagotomy in addition to Hex. With room air apneas, during the apnea cycle, there were increases in mean arterial pressure (MAP; from baseline of 108 ± 4 to 124 ± 6 Torr, P < 0.01), plasma norepinephrine (from 681 ± 99 to 1,825 ± 578 pg/ml, P < 0.05), and epinephrine (from 191 ± 67 to 1,245 ± 685 pg/ml, P < 0.05) but decreases in cardiac output (CO; from 3.3 ± 0.6 to 2.4 ± 0.3 l/min, P < 0.01) and cervical sympathetic nerve activity. With O2supplementation relative to baseline, apneas were associated with small increases in MAP (from 112 ± 4 to 118 ± 3 Torr, P < 0.01) and norepinephrine (from 675 ± 97 to 861 ± 170 pg/ml, P< 0.05). After Hex, apneas with room air were associated with small increases in MAP (from 103 ± 6 to 109 ± 6 Torr, P < 0.05) and epinephrine (from 136 ± 45 to 666 ± 467 pg/ml, P < 0.05) and decreases in CO (from 3.6 ± 0.4 to 3.2 ± 0.5 l/min, P < 0.05). After Hex, apneas with O2 supplementation were associated with decreased MAP (from 107 ± 5 to 100 ± 5 Torr, P < 0.05) and no other changes. After vagotomy + Hex, with room air and O2 supplementation, apneas were associated with decreased MAP (from 98 ± 6 to 76 ± 7 and from 103 ± 7 to 95 ± 6 Torr, respectively, both P < 0.01) but increased CO [from 2.7 ± 0.3 to 3.2 ± 0.4 l/min ( P < 0.05) and from 2.4 ± 0.2 to 2.7 ± 0.2 l/min ( P < 0.01), respectively]. We conclude that sympathoadrenal activation is the major pressor mechanism during apneas. Cervical sympathetic nerve activity does not reflect overall sympathoadrenal activity during apneas. Hypoxemia is an important but not the sole trigger factor for sympathoadrenal activation. There is an important vagally mediated reflex that contributes to the pressor response to apneas.

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Effect of Pneumoperitoneum on Cervical Sympathetic Nerve Activity and Hemodynamics

Anesthesiology ◽

10.1097/00000542-199809120-00059 ◽

1998 ◽

Vol 89 (Supplement) ◽

pp. 647A

Author(s):

H Aono ◽

A Takeda ◽

K Shinohara ◽

K T Benson ◽

H Goto

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Cervical Sympathetic ◽

Cervical Sympathetic Nerve

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Gender-related differences in the sympathetic vasoconstrictor drive of normal subjects

Clinical Science ◽

10.1042/cs20060288 ◽

2007 ◽

Vol 112 (6) ◽

pp. 353-361 ◽

Cited By ~ 74

Author(s):

Andrew J. Hogarth ◽

Alan F. Mackintosh ◽

David A. S. G. Mary

Keyword(s):

Blood Flow ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Muscle Sympathetic Nerve Activity ◽

Cold Pressor ◽

Normal Subjects ◽

Isometric Handgrip ◽

Nerve Activity ◽

Vasoconstrictor Response ◽

Baroreceptor Reflex Sensitivity

The risk of cardiovascular disease has been linked to sympathetic activation and its incidence is known to be lower in women than in men. However, the effect of gender on the sympathetic vasoconstrictor drive has not yet been established. In the present study, we investigated whether there is a gender difference in MSNA (muscle sympathetic nerve activity) and blood flow, and to determine the mechanisms involved. We examined 68 normal subjects, 34 women and 34 men, matched for age, BMI (body mass index) and waist circumference. MSNA was measured as the mean frequency of single units (s-MSNA) and as multi-unit bursts (m-MSNA) from the peroneal nerve simultaneously with its supplied muscle CBF (calf blood flow). Women had lower (P=0.0007) s-MSNA (24±2.0 impulses/100 cardiac beats) than men (34±2.3 impulses/100 cardiac beats), and a greater baroreceptor reflex sensitivity controlling efferent sympathetic nerve activity than men. The sympathetic activity was inversely and directly correlated respectively, with CBF (P=0.03) and CVR (calf vascular resistance; P=0.01) in men only. The responses of an increase in CVR to cold pressor and isometric handgrip tests were significantly smaller in women (P=0.002) than in men, despite similar increases in efferent sympathetic nerve activity. Women had a lower central sympathetic neural output to the periphery, the mechanism of which involved differences in central and reflex control, as well as a lower vasoconstrictor response to this neural output. It is suggested that this may partly explain the observed lower incidence of cardiovascular events in women compared with men.

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Effect of cervical sympathetic trunk transection on renal sympathetic nerve activity in rats

Physiological Research ◽

10.33549/physiolres.931186 ◽

2009 ◽

pp. 77-82

Author(s):

T Ikeda ◽

H Hirakawa ◽

T Kemuriyama ◽

Y Nishida ◽

T Kazama

Keyword(s):

Blood Pressure ◽

Local Anesthetic ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Tibial Nerve ◽

Sympathetic Trunk ◽

Nerve Activity ◽

Cervical Sympathetic Trunk ◽

Arterial Blood ◽

Cervical Sympathetic

Stellate ganglion blockade (SGB) with a local anesthetic increases muscle sympathetic nerve activity in the tibial nerve in humans. However, whether this sympathetic excitation in the tibial nerve is due to a sympathetic blockade in the neck itself, or due to infiltration of a local anesthetic to adjacent nerves including the vagus nerve remains unknown. To rule out one mechanism, we examined the effects of cervical sympathetic trunk transection on renal sympathetic nerve activity (RSNA) in anesthetized rats. Seven rats were anesthetized with intraperitoneal urethane. RSNA together with arterial blood pressure and heart rate were recorded for 15 min before and 30 min after left cervical sympathetic trunk transection. The baroreceptor unloading RSNA obtained by decreasing arterial blood pressure with administration of sodium nitroprusside was also measured. Left cervical sympathetic trunk transection did not have any significant effects on RSNA, baroreceptor unloading RSNA, arterial blood pressure, and heart rate. These data suggest that there was no compensatory increase in RSNA when cervical sympathetic trunk was transected and that the increase in sympathetic nerve activity in the tibial nerve during SGB in humans may result from infiltration of a local anesthetic to adjacent nerves rather than a sympathetic blockade in the neck itself.

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Sympathomimetic pressor responses to thyrotropin-releasing hormone in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1986.251.1.h86 ◽

1986 ◽

Vol 251 (1) ◽

pp. H86-H92 ◽

Cited By ~ 2

Author(s):

J. Mattila ◽

R. D. Bunag

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Cardiovascular Responses ◽

Splanchnic Nerve ◽

Sympathetic Nerves ◽

Thyrotropin Releasing Hormone ◽

Nerve Activity ◽

Releasing Hormone ◽

Pressor Responses ◽

Cervical Sympathetic

Cardiovascular responses to centrally administered thyrotropin-releasing hormone (TRH) were studied in urethan-anesthetized rats to allow continuous recording of attendant changes in sympathetic nerve activity. Intracerebroventricular infusions of TRH (0.05-5.0 micrograms) consistently increased not only blood pressure and heart rate, but also spike frequency in splanchnic, renal, or cervical sympathetic nerves. Parasympathetic inhibition seemed unlikely because TRH responses were unaltered by cholinergic blockade with atropine, and efferent vagal nerve firing, instead of being reduced, was actually increased by TRH. An increased secretion of endogenous vasopressin also appeared unlikely, since TRH responses were essentially unaffected by either hypophysectomy or pretreatment with a vasopressin antagonist. Inasmuch as pharmacological ganglion blockade with pentolinium eliminated increases in splanchnic nerve firing but reduced the attendant tachycardia by only 50%, residual tachycardia after ganglion blockade was considered partly due to persistent sympathetic cardioaccelerator tone. On the other hand, because pressor responses to TRH were always accompanied by increased sympathetic nerve firing and were completely abolished after pentolinium-induced ganglioplegia, they were attributed solely to sympathetic hyperactivity.

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