sympathectomy created imbalance of autonomic activity and functional changes of the intrathoracic organs

Surgical thoracic sympathectomy such as ESD (endoscopic thoracic sympathectic denervation) or heart transplantation can result in an imbalance between the sympathetic and parasympathetic activities and result in functional changes in the intrathoracic organs.

Therefore, the procedures affecting sympathetic nerve functions, such as epidural anesthesia, ESD, and heart transplantation, may cause an imbalance between sympathetic and parasympathetic activities (1, 6, 16, 17). Recently, it has been reported that ESD results in functional changes of the intrathoracic organs.


In conclusion, our study demonstrated that ESD adversely affected lung function early after surgery and the BHR was affected by an imbalance of autonomic activity created by bilateral ESD in patients with primary focal hyperhidrosis.
Journal of Asthma, 46:276–279, 2009
http://informahealthcare.com/doi/abs/10.1080/02770900802660949

"changes in old age show some similarities with those following chronic sympathectomy" "Prejunctional supersensitivity to norepinephrine after sympathectomy or cocaine treatment."

"For the tracheobronchial tree. surgical (sympathectomy) and chemical (with 6-hydroxydopamine or reserpine) interventions lead to histological disappearance of the NA and NPY." (p.435)

"Prejunctional supersensitivity to norepinephrine after sympathectomy or cocaine treatment." (p. 410)

"Following chronic sympathectomy, substance P expression in presumptive sensory nerves....and NPY-expression in parasympathetic nerves ...to autonomically innervated tissues have both been shown to increase... Experiments using NGF and anti-NGF antibodies (Kessler et al., 1983) have suggested that competition between sympathetic and sensory fibers for target-derived growth factors could explain these apparently compensatory interactions,..." (p. 33)

"Since changes in old age show some similarities with those following chronic sympathectomy, it is tempting to consider whether alterations in one group of nerves in tissues with multiple innervations trigger reciprocal changes in other populations of nerves, perhaps through the mechanism of competition for common, target-produced growth factors. The nature of these changes is such that they could be nonadaptive and even destabilizing of cardiovascular homeostasis. (p. 34)

Impairment of sympathetic and neural function has been claimed in cholesterol-fed animals (Panek et al., 1985). It has also been suggested that surgical sympathectomy may be useful in controlling atherosclerosis in certain arterial beds (Lichter et al., 1987). Defective cholinergic arteriolar vasodilation has been claimed in atherosclerotic rabbits (Yamamoto et al., 1988) and, in our laboratory, we have recently shown impairment of response to perivascular nerves supplying the mesenteric, hepatic, and ear arteries of Watanabe heritable hyperlipidemic rabbits (Burnstock et al., 1991).
   Loss of adrenergic innervation has been reported in alcoholism (Low et al., 1975), amyloidosis (Rubenstein et al., 1983), orthostatic hypotension (Bannister et al., 1981), and subarachnoid haemorrhage (Hara and Kobayashi, 1988). Recent evidence shows that there is also a loss of noradrenergic innervation of blood vessels supplying malignant, as compared to benign, human intracranial tumours (Crockard et al., 1987). (p. 14)  

Vascular Innervation and Receptor Mechanisms: New    Perspectives 

Rolf Uddman

Academic Press, 2 Dec 2012 - Medical - 498 pages