Sympathetic denervation

Hart MN, Heistad DD, Brody Ml. Effect of chronic hypertension and sympathetic denervation on waMumen ratio of cerebral vessels. Hypertension 1980 2(4) 419 23. 

In patients with hypotension due to high thoracic spinal cord transections (resulting in an essentially complete sympathetic denervation), loss of sympathetic vasomotor control can be compensated by administration of sympathomimetics. 

Innervation. NET 6-[18F]FDA was used in patients with PD with orthostatic hypotension. It was ascertained that PD with orthostatic hypotension features inter alia sympathoneural failure and cardiac sympathetic denervation, independent of levodopa treatment [203]. Based on a profoundly decreased LV myocardial 6-[18F]FDA-derived radioactivity 4 years before the onset of symptoms of PD, the same group hypothesize that cardiac noradrenergic denervation may occur early in the pathogenesis of PD [204,205]. 

J.P. Moak, B. Eldadah, C. Holmes, S. Pechnik, D.S. Goldstein, Partial cardiac sympathetic denervation after bilateral thoracic sympathectomy In humans. Heart Rhythm. 2 (2005) 602-609. 

D.S. Goldstein, Y. Sharabi, B.l. Karp, O. Bentho, A. Saleem, K. Pacak, G. Eisenhofer, Cardiac sympathetic denervation preceding motor signs in Parkinson disease, Clin. Auton. Res. 17 (2007) 118-121. 

Neurogenic renal vasoconstriction, with consequent activation of the renin-angio-tonin mechanism, is not a major factor in most cases of neurogenic hypertension evidence for this is seen in the limited fall in blood pressure which follows renal denervation (41, 54) and the failure of prior nephrectomy to alter the pressor response to moderator nerve section (95). However, neurogenic renal vasoconstriction may be adequate to produce a sustained hypertension after other body structures have been sympathetically denervated (42, 44)) and it is possible that neurogenic renal vasoconstriction may play a significant role in the development of essential hypertension. 

Another possible cause of respiratory-related disturbances in Parkinson s patients may be related to changes in cardiac autonomic control during sleep (134). Functional imaging studies reported the occurrence of selective cardiac sympathetic denervation in Parkinson s patients (135), though the clinical significance of this finding is still undetermined. 

Cosentino M, Marino F, De Ponti F et al (1995) Tonic modulation of neurotransmitter release in the guinea-pig myenteric plexus effect of mu and kappa opioid receptor blockade and of chronic sympathetic denervation. Neurosci Lett 194 185-8 Costa M, Majewski H (1988) Facilitation of noradrenaline release from sympathetic nerves through activation of ACTH receptors, B-adrenoceptors and angiotensin II receptors. Br J Pharmacol 95 993-1001... 

Krum H, Schlaich M, Whitboum P, et al. Catheter-based renal sympathetic denervation for resistant hypertension a multiplecentre safety and proof-of-principle cohort study. Lancet. 2009 373 1275-1281. 

Ptosis resulting from sympathetic denervation, as in Horner s syndrome, may respond to topical phenylephrine. Dramatic effects on the uneven palpebral apertures are sometimes observed (see Figure 23-15). 

Phenylephrine can also be used as a diagnostic test for Horner s syndrome (see Chapter 22). Phenylephrine in the 1% concentration can markedly dilate the pupil with postganglionic sympathetic denervation. It causes minimal or no dilation in the normal eye. If the lesion is central or preganglionic, the affected pupil responds in a manner similar to the normal eye because denervation hypersensitivity is minimal or absent. 

Apraclonidine Test. Apraclonidine 1% has shown promise in testing for Horner s syndrome. The drug should be instilled in both eyes. Significant pupillary dilation occurs in the eye with Horner s syndrome, whereas little or no dilation occurs in the normal eye. The up-regulation of a-receptors that occurs with sympathetic denervation in Horner s syndrome appears to unmask apraclonidine s tti effect in the eye with Homer s syndrome. 

Phenylephrine Test. If hydroxyamphetamine is not readily available, an alternative is to use a weak 1% solution of phenylephrine to demonstrate that the pupil in postganglionic Horner s syndrome has denervation sensitivity. Solutions of 1% phenylephrine do not dilate the normal pupil, but in the presence of sympathetic denervation may... 

Deferrari GM, Locati EH, Priori SG, Schwartz PJ. 1995. Left cardiac sympathetic denervation in long QT syndrome patients. J. Interv. Cardiol. 8 776-81... 

During adrenergic neuron blockade with guanadrel, effector cells become supersensitive to norepinephrine. The supersensitivity is similar to that prodnced by postganglionic sympathetic denervation. 

The cause of the mydriatic action of cocaine is obscure. It is well known that cocaine potentiates the action of epinephrine (e.g., on blood pressure) and of other sympathomimetic amines which contain the catechol nucleus (62). It is also known that cocaine inhibits amine oxidase (63) so that it is tempting to attribute the mydriatic action of cocaine to the inhibition of this enzyme, which occurs in the iris (54) and is known to catalyze the oxidation of the sympathetic transmitter. At the same time it must be admitted that amine oxidase may not be the only enzyme concerned in the destruction of norepinephrine and epinephrine liberated at the peripheral endings of sympathetic nerves (64). All that can be said is that the sympathomimetic effects of cocaine, like mydriasis, are almost certainly not due to a direct action on effector cells resembling that of epinephrine and norepinephrine, since cocaine is ineffective on sympathetically denervated structures. It would seem that cocaine achieves mydriasis by some indirect action, and the likeliest explanation is that it inhibits some enzyme system concerned with the inactivation of the sympathetic transmitter. 

Lee J, Turner JR (2016) Raising the bar in renal sympathetic denervation research and reporting. J CUn Hypertens (Greenwich) 18 89-94... 

In 1913, Leriche and Jaboulay (47) first described and tested the concept of sympathetic denervation as therapy for ischemia secondary to arterial occlusive disease. Despite less than optimal initial results, others soon applied the technique with better long-term results, and by the mid-1920s, sympathectomy had emerged as the only alternative to amputation for severe arterial occlusive disease. By the early 1960s, advances in pain control and arterial reconstruction combined with considerable debate over the true value of sympathectomy led to a substantial decline in its use. Today, sympathectomy remains a well-described technique with a diminishing number of applications. 

Ryan ML, Hedrick MS, Pizarro J, Bisgard GE. Effects of carotid body sympathetic denervation on ventilatory accbmatization to hypoxia in the goat. Respir Physiol 1995 99 215-224. 

Fletcher EC, Lesske J, Culman J, Miller CC, Unger T. Sympathetic denervation blocks blood pressure elevation in episodic hypoxia. Hypertension 1992 20 612-619. 

Kim JM, Stevenson CE, Mathewson HS. H5 ertensive reactions to phenylephrine eyedrops in patients with sympathetic denervation. Am J Ophthalmol 1978 85(6) 862-8. 

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