Peripheral sympathectomy and adrenal medullectomy do not alter cerebrospinal fluid norepinephrine

Peskind, Elaine R.; Raskind, Murray A.; Wilkinson, Charles W.; Flatness, David E.; Halter, Jeffrey B.

doi:10.1016/0006-8993(86)91600-8

Cited by 27 publications

(6 citation statements)

References 35 publications

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“…If an analogous situation occurred in humans, then a generalized loss of sympathetic post-ganglionic innervation in patients with PAF could result in correlated decreases in cerebrospinal fluid and plasma levels of noradrenaline, as in the present study, without necessarily indicating a central noradrenergic deficiency state. No data exist in humans about the actual contributions of sources outside the central nervous system to cerebrospinal fluid levels of either noradrenaline or dihydroxyphenylglycol, and the literature with regard to laboratory animals is inconsistent [28,29]. Accordingly, the present results cannot be taken as providing unequivocal support for central noradrenergic deficiency in PAF.…”

Section: Discussioncontrasting

confidence: 60%

Cerebrospinal fluid levels of catechols in patients with neurogenic orthostatic hypotension

et al. 2003

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In multiple system atrophy (MSA) and pure autonomic failure (PAF), orthostatic hypotension (OH) results from deficient noradrenaline release from sympathetic nerves during standing. Post-mortem findings have indicated loss of central noradrenergic cells in both diseases. The present study sought in vivo neurochemical evidence for central noradrenergic deficiency in patients with OH due to MSA or PAF. A total of 28 patients with OH (18 with MSA; 10 with PAF) had cerebrospinal fluid and blood sampled for levels of noradrenaline and its neuronal metabolite dihydroxyphenylglycol. A control group of 44 subjects included 10 elderly normal volunteers, 10 patients with Alzheimer's disease, 18 patients with dysautonomia (postural tachycardia syndrome or neurocardiogenic syncope) and six patients with MSA in the absence of OH. Patients with OH had lower cerebrospinal fluid concentrations of noradrenaline (0.53+/-0.07 nmol/l) and dihydroxyphenylglycol (6.52+/-0.46 nmol/l) than did control subjects (0.90+/-0.09 and 9.64+/-0.46 nmol/l respectively; P =0.0001). The MSA+OH group had higher plasma levels of both catechols (noradrenaline, 1.31+/-0.16 nmol/l; dihydroxyphenylglycol, 5.08+/-0.43 nmol/l) than did the PAF group (noradrenaline, 0.38+/-0.08 nmol/l; dihydroxyphenylglycol, 2.53+/-0.30 nmol/l; P <0.001), despite similarly low cerebrospinal fluid levels. Among MSA patients, those with OH had lower cerebrospinal fluid levels of noradrenaline and dihydroxyphenylglycol than those without OH (noradrenaline, 1.71+/-0.64 nmol/l; dihydroxyphenylglycol, 10.41+/-1.77 nmol/l respectively; P =0.006). The findings are consistent with central noradrenergic deficiency in both MSA+OH and PAF. In MSA, central noradrenergic deficiency seems to relate specifically to OH.

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Section: Discussioncontrasting

confidence: 60%

Cerebrospinal fluid levels of catechols in patients with neurogenic orthostatic hypotension

et al. 2003

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“…This explanation cannot account, however, for the absence of increases in CSF NE during hypotension in ganglion-blocked subjects, since central noradrenergic tone should have been stimulated reflexively. Peskind et al ( 1986) recently reported that peripheral sympathectomy of rats at 1 week of age using guanethidine, followed by adrenal medullectomy at 7 weeks, did not affect CSF NE measured at 12 weeks but did decrease plasma NE. drawn from these findings, that peripheral sources of NE probably do not contribute significantly to CSF NE, conflicts with our conclusions based on the present results.…”

Section: Discussionmentioning

confidence: 97%

Effect of Ganglion Blockade on Cerebrospinal Fluid Norepinephrine

Goldstein

Zimlichman

Kelly

et al. 1987

Journal of Neurochemistry

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The source of norepinephrine (NE) in CSF has been unclear. It has been suggested that CSF NE indicates central neural noradrenergic tone and is determined differently from plasma NE. If CSF NE depended specifically on NE release in the CNS, then interference with ganglionic neurotransmission would be expected to decrease plasma NE but not CSF NE. Hypotension caused by ganglionic blockade might be expected to increase CSF NE reflexively. We infused the ganglion blocker, trimethaphan, intravenously into anesthetized dogs and measured the effects on mean arterial blood pressure (MAP) and on cisterna magna CSF levels of NE. The results were compared with those obtained on administration of saline, clonidine (2 micrograms/kg), yohimbine (0.25 mg/kg), or nitroprusside and with those obtained when hypotension during ganglion blockade was prevented by concurrent treatment with phenylephrine. Trimethaphan decreased MAP by 40%, arterial NE by 64%, and CSF NE by 61%. Nitroprusside administered intravenously to produce the same 40% depressor response increased arterial NE by 612% and CSF NE by 155%. Prevention of ganglion blockade-induced hypotension using phenylephrine did not prevent the decrease in CSF NE caused by trimethaphan, and when phenylephrine was discontinued, the resulting hypotension was not associated with increases in CSF NE. The similar decreases in plasma NE and CSF NE during ganglionic blockade, and the abolition of reflexive increases in CSF NE during hypotension in ganglion-blocked subjects, cast doubt on the hypothesis that CSF NE indicates central noradrenergic tone and are consistent instead with at least partial derivation of CSF NE from postganglionic sympathetic nerve endings.

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“…Nonetheless, the results do demonstrate that under consistent and closely controlled isocaloric conditions, chronic ethanol consumption did alter E and NE plasma concentrations during prolonged imposed abstinence, under basal conditions and in response to transfer to a novel environment. The brain noradrenergic system and the peripheral sympathetic system are functionally integrated, plasma NE concentrations generally correlate well with cerebrospinal fluid (CSF) NE, and this correlation is not due to peripheral catecholamines gaining access to CSF (Peskind et al, 1986;Roy et al, 1988;Ziegler et al, 1977). Plasma NE and E responses to stress are mediated at least in part by noradrenergic mechanisms in the brain, and stress-induced increases in plasma NE and E concentrations have been demonstrated to be consistent with corresponding changes in extracellular concentrations of NE in the hypothalamic paraventricular nucleus which integrates many stress responses (Tjurmina et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Chronic daily ethanol and withdrawal: 6. Effects on rat sympathoadrenal activity during “abstinence”

Rasmussen¹,

Wilkinson²,

Raskind³

2006

Alcohol

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We have reported that repetitive daily ethanol consumption increased anxiety-like behavior in rats 4 weeks after ethanol consumption had ceased, consistent with the persistently increased anxiety exhibited by abstinent alcoholics. Increased anxiety is associated with sym-pathoadrenal activation, so we have now also investigated ethanol-induced persistent changes in basal and stress-induced plasma epinephrine (E) and norepinephrine (NE) levels. Male Sprague-Dawley rats received liquid diet containing ethanol versus pair-fed isocaloric control liquid diet for 9 weeks. After 5 weeks' subsequent ''abstinence'' (i.e., no ethanol in the diet), the control rats exhibited low basal plasma E and NE, which were both increased by 150-300% within 5 min after transfer to a novel cage in a novel room, returning toward basal levels within 15 min. ''Abstinent'' ethanol-treated rats exhibited elevated basal E levels (195% of controls, P < .05), which were not significantly altered by transfer to novel environment; basal NE levels tended (P < .07) to be elevated and likewise were not altered by novel environment. These results suggest that daily ethanol consumption can induce persistent increases in sympathoadrenal activation during subsequent ''abstinence,'' which are relatively refractory to further stimulation.

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Peripheral sympathectomy and adrenal medullectomy do not alter cerebrospinal fluid norepinephrine

Cited by 27 publications

References 35 publications

Cerebrospinal fluid levels of catechols in patients with neurogenic orthostatic hypotension

Cerebrospinal fluid levels of catechols in patients with neurogenic orthostatic hypotension

Effect of Ganglion Blockade on Cerebrospinal Fluid Norepinephrine

Chronic daily ethanol and withdrawal: 6. Effects on rat sympathoadrenal activity during “abstinence”

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