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PubMed1985

Effects of chemical sympathectomy on dopamine and noradrenaline content of the dog gastrointestinal tract.

The content of dopamine and noradrenaline in the mucosa-submucosa and muscular layers of different gastrointestinal areas of the dog, and its modification by 6-hydroxydopamine or pargyline plus 6-hydroxydopamine was studied by means of high pressure liquid chromatography with electrochemical detection. The amounts of dopamine and noradrenaline show a cephalocaudal increase but their physiological levels were rather low when compared with those reported in other tissues. This finding was consistent with the sparse noradrenergic innervation classically described for the gut with histochemical methodologies. On the basis that noradrenergic neurones are considered more susceptible to 6-hydroxydopamine than dopaminergic neurones, a difference abolished by previous treatment with pargyline, our findings did not suggest the existence of dopaminergic neurones in the gastrointestinal tract of the dog. In the muscular layer of the duodenum, jejunum and ileum it was observed that catecholamine depletion by both treatments was smaller than that obtained in the mucosa-submucosa. Due to the resistance to both kinds of chemical sympathectomy exhibited by the dopamine content, the existence of dopamine-containing enterochromaffin cells is proposed in the mucosa-submucosa of different portions of the stomach and small intestine.

Animals↗
PubMed1982

The effect of chemical sympathectomy on mitochondrial function in the ischaemic and reperfused myocardium.

1 Isolated rabbit hearts were perfused aerobically for 120 min, made ischaemic for 90 min, or made ischaemic for 90 min and then reperfused for 30 min. 2 Some rabbits were pretreated with 6-hydroxydopamine (6-OHDA), given as three separate intravenous doses of 30, 20 and 20 mg/kg, 20 to 48 h before they were killed; others (controls) received saline according to the same regime. 3 Mitochondria were harvested from left ventricular homogenates and their function assessed by measuring state 3O2 consumption (state 3 QO2), respiratory control index (RCI), phosphate: oxygen ratio (ADP:O), Ca2+ content, and ATP-producing activity. In other experiments peak left ventricular developed tension was recorded. 4 In hearts from saline-treated animals, mitochondrial state 3 QO2, RCI and ATP producing activities were reduced after global ischaemia, with or without reperfusion. There was a small gain in mitochondrial Ca2+ after ischaemia, and a large gain upon reperfusion. 5 6-OHDA pretreatment provided some protection against the effects of ischaemia and reperfusion on mitochondrial function and on peak developed tension. 6 It was concluded that chemical sympathectomy with 6-OHDA does not duplicate the effect of prolonged beta-adrenoceptor blockade in protecting mitochondrial function against the deleterious effects of ischaemia and reperfusion.

Adenosine Triphosphate↗
PubMed2005

Chemical sympathectomy inhibits periodontal disease in Fischer 344 rats.

OBJECTIVE: The responsiveness of the sympathetic nervous system (SNS) and the hypothalamic--pituitary--adrenal (HPA) axis plays a major role in immune regulation and for the outcome of infections and inflammatory disorders. This study was designed to investigate whether chemical SNS denervation with the noradrenaline-selective neurotoxic drug 6-hydroxydopamine (6-OHDA), which destroys peripheral noradrenaline terminals, would influence immune responses to Gram-negative bacterial lipopolysaccharide (LPS) stimulation, and the progression of ligature-induced periodontal disease in Fischer 344 rats. MATERIAL AND METHODS: 6-OHDA (40--60 microg/kg) or vehicle was injected intraperitoneally (i.p.) on days 1, 3 and 5, 10 days before application of the ligatures, and thereafter weekly in doses of 80 microg/kg. Periodontal disease was assessed when the ligatures had been in place for 49 days. At 24 and 2 h before decapitation, all rats received LPS (150 microg/kg i.p.) to induce a robust immune and HPA axis response. RESULTS: The 6-OHDA-treated rats showed significantly reduced bone loss as measured by digital X-rays (p< 0.01), and enhanced levels of the cytokines transforming growth factor-beta (p=0.05) and interleukin-6 (p=0.05), as well as the HPA axis derived hormone corticosterone (p=0.01), induced by LPS stimulation. CONCLUSIONS: 6-OHDA-induced chemical sympathectomy inhibits ligature-induced periodontal disease in this model. This effect may be attributable to the well-documented ability of the SNS to regulate immune system function primarily via the adrenergic neurotransmitter noradrenaline released at sympathetic nerve terminals. The enhanced HPA axis activation may be a compensatory response that reduces the T helper (Th)2 to Th1 skewing effect of treatment with 6-OHDA.

Alveolar Bone Loss↗
PubMed1976

Chemical sympathectomy of interscapular brown adipose tissue.

Adult non-cold adapted rats were injected with 6-hydroxydopamine (6-OHDA) or saline and their interscapular brown adipose tissue (BAT) was removed after appropriate periods of time. Fluorescence histochemistry of control BAT demonstrated the presence of an extensive network of varicose fibers among the adipocytes and at the blood vessels. This was confirmed by electron microscopy which also revealed large and small dense core vesicles sparsely distributed in axons and terminals indicating the presence of noradrenaline (NA). After 6-OHDA injection the fluorescence from varicosities was abolished both among the adipocytes and at the vessels. Thus, chemical sympathectomy was more effective than surgical- or immunosympathectomy, which spare the innervation of adipocytes. Parallelling the disappearance of fluorescence was a significant decrease of measurable NA. During recovery the extractable NA increased before the reappearance of fluorescent varicosities. This could be explained by transmitter accumulation in the nervetrunks within the tissue, which, in general, appeared unaffected by 6-OHDA. A large number of cells with a strong yellowish fluorescence distributed through the BAT was unaffected by 6-OHDA. There was no evidence for the presence of intrinsic ganglia.

Adipose Tissue, Brown↗
PubMed1983

The effect of lumbar sympathectomy on fiber composition, contractility of skeletal muscle and regulation of central circulation in dogs.

It has been speculated upon that the sympathetic activity might be of significance for fiber composition in skeletal muscle and by similar features indirectly affecting muscle contractility and regulation of circulation. To further study this hypothesis unilateral lumbar sympathectomy from L-2 and down was applied on 5 female dogs. After 14 weeks the gracilis muscle on the sympathectomized and the control side as well were examined for their muscle fiber compositions, endurance capacity and how heart rate and blood pressure responses were affected. Muscle fiber composition decreased to 28% slow twitch fibers as compared to 41% on the control side (p less than 0.01). The relative cross-sectional area of the fast twitch fibers increased simultaneously from 57 (control side) to 71% (p less than 0.05). Endurance performance measured as contraction time at 50% of peak tension decreased from 55 to 29 s (p less than 0.05). On an individual bases including both control and sympathectomized muscles it was found that heart rate increased with percent fast twitch muscle fibers (p less than 0.01) and a tendency was present for a similar relationship between blood pressure and fiber types (p less than 0.1).

Animals↗
PubMed1990

Influence of renal sympathectomy, sodium depletion and prostaglandin synthetase inhibition on prostaglandin production and [3H]PGE2 binding characteristics in rat kidney.

The effects of renal sympathectomy (unilateral, renal microsurgical denervation), sodium depletion (hypovolaemia) and prostaglandin synthetase inhibition on the rate of prostaglandin synthesis and [3H]PGE2 binding characteristics were studied in the rat kidney. The intrarenal rate of prostaglandin synthesis was measured by monitoring the urinary excretion of 6-keto-PGF1 alpha, the stable hydration product of prostacyclin. Dietary sodium restriction was associated with a 99% decrease in urinary sodium excretion (P less than 0.001) and a 17% decrease of urine volume (n.s.). Renal denervation or sodium deprivation changed neither the rate of excretion of 6-keto-PGF1 alpha nor the density or affinity of [3H]PGE2 binding sites as compared to control. However, in sodium-depleted rats, prostaglandin synthesis inhibition, induced by naproxen, decreased the urinary excretion of 6-keto-PGF1 alpha by 40% (P = 0.011) and increased the number of [3H]PGE2 binding sites by almost 30% (P = 0.031) with no change in binding affinities as compared with sodium-depleted controls. In contrast, sulindac was not able to suppress the renal synthesis and excretion of 6-keto-PGF1 alpha, and did not modulate the [3H]PGE2 binding characteristics. The lack of effect on the excretion of 6-keto-PGF1 alpha and on the [3H]PGE2 binding characteristics supports the view that sulindac spares renal prostaglandin synthesis.

Animals↗
PubMed1990

Secretory effects of 5-hydroxytryptamine following neonatal sympathectomy in rat parotid gland.

Unilateral sympathetic denervation of rat parotid glands was performed within 4 h after birth. Nine weeks later the glands were used for in-vitro studies of amylase secretion, and 86Rb+ was used as a marker for potassium efflux. The non-denervated contralateral glands served as controls. The tissue concentrations of 5-hydroxytryptamine and its metabolite 5-hydroxyindole acetic acid were also measured. 5-Hydroxytryptamine caused a significant dose-dependent increase in amylase secretion, which was inhibited by methysergide. There was no difference between controls and denervated glands. 5-Hydroxytryptamine was without effect on potassium efflux from either denervated or control glands. The sympathectomy caused increased levels of 5-hydroxytryptamine and 5-hydroxyindole acetic acid as compared with contralateral controls. The results suggest that 5-hydroxytryptamine influences the two main secretory processes in rat parotid gland differently. A significant amylase discharge was seen following 5-hydroxytryptamine stimulation, whereas no effect was seen on 86Rb+ efflux. Although it is also proposed that there are no 5-hydroxytryptamine-associated nerves in the superior cervical ganglion innervating parotid tissue, it seems that there is a complex connection between the sympathetic pathway and the serotoninergic system.

Amylases↗
PubMed2000

Chemical sympathectomy alters cytotoxic T lymphocyte responses to herpes simplex virus infection.

Numerous studies have sought to delineate the impact of neuroendocrine function on overall immune responsiveness. Using various murine models, we and others have previously shown that both adrenal-dependent and adrenal-independent mechanisms regulate components of the primary and memory cellular immune responses to herpes simplex virus type 1 (HSV-1) infection. We have extended these studies by determining the impact of 6-hydroxydopamine (6-OHDA)-induced peripheral sympathetic denervation on these responses. C57BL/6 mice treated with 6-OHDA (200 mg/kg) were inhibited in their ability to generate primary, HSV-specific cytotoxic T lymphocytes (CTL) in response to HSV infection. Sympathectomy also suppressed the activation and function of HSV-specific memory CTL (CTLm). In addition, administration of 6-OHDA resulted in a transient but substantial increase in levels of circulating corticosterone and hypothalamic Fos expression. Together, these findings suggest that peripheral sympathetic denervation may modulate immune function via activation of the hypothalamic-pituitary-adrenal (HPA) axis.

Animals↗
PubMed1982

Parotid degeneration secretion of amylase in vitro in the rat following sympathectomy.

After extirpation of the superior cervical ganglion in the rat a degeneration secretion of amylase occurs in an in vitro preparation of the parotid gland. It can be detected about 14 h after the sympathectomy, reaches a maximum after about 17 h and then slowly subsides. It is abolished by atenolol, but not by dihydroergotamine or atropine, nor by tetrodotoxin. From this it is concluded that the phenomenon is due to an action mainly on beta 1-adrenoceptors exerted by noradrenaline, which is released from the degenerating sympathetic nerves at the neuro-glandular junctions, independently of propagated nerve impulses.

Amylases↗
PubMed1988

Influences of short-term sympathectomy on the composition of proteins in rat parotid saliva.

The protein constituents in parasympathetically evoked saliva from normal and short-term sympathectomized parotid glands were compared. There was a reduction in all proline-rich proteins (PRP) in the saliva following sympathectomy. The decrease was quantified for acidic PRP by high-performance ion-exchange chromatography, which showed an increase in the ratio of amylase to other proteins. These results suggest that sympathetic impulses influence the synthesis of PRP and amylase in opposite directions.

Amylases↗
PubMed1989

A comparison between changes in rat parotid protein composition 1 and 12 weeks following surgical sympathectomy.

One week after surgical sympathectomy the amylase and protein concentrations of parotid glands were increased by 250 and 51% respectively. Whilst these concentration changes had partly returned to normal after 12 weeks, major differences still remained in the protein composition of parotid glands. Anion-exchange chromatography showed that proline-rich proteins were progressively reduced and that the relative proportions of other proteins changed variably. These results indicate that normal synthesis of proline-rich proteins requires on-going stimulation of the cells via the sympathetic nerve. In the absence of sympathetic nerve activity there was initially an increased synthesis of amylase which then returned towards normal.

Amylases↗
PubMed1974

Degeneration secretion of saliva in the rat following sympathectomy.

1. After previous extirpation of the superior cervical ganglion saliva was found to flow from the cannulated submaxillary duct of rats under chloralose anaesthesia. The secretion started 13-14.5 hr after sympathectomy, increased gradually in rate and then slowed down and ceased, lasting for about 12 hr.2. Injection of alpha- or beta-adrenoreceptor blocking drugs reduced the flow and a combination of both types of drugs abolished it. It is concluded that the secretion was caused by noradrenaline released from the degenerating nerves, and that the phenomenon is an example of the degeneration activity described in other preparations as an effect of section of post-ganglionic autonomic nerves.3. A similar, but less pronounced, secretion was found in the parotid gland of the rat.

Adrenergic alpha-Antagonists↗
PubMed1988

The effects of atropine and chronic sympathectomy on maximal parasympathetic stimulation of parotid saliva in rats.

1. The effects of stimulating the postganglionic parasympathetic nerve to the parotid gland, the auriculo-temporal nerve, continuously at 40 Hz for 80 min have been assessed on the flow of saliva and its amylase content during each 10 min period and on the glandular morphology at the end of the stimulation, in female Sprague-Dawley rats under chloralose anaesthesia. Adrenergic responses were blocked by prior administration of dihydroergotamine (1 mg/kg I.P.) and propranolol (1 mg/kg I.P.). The contralateral unstimulated parotid gland from each animal was used for morphological control purposes. 2. In normal animals there was a copious flow of saliva reaching 3 ml or more in 80 min. It was well maintained after a gradual small decline and the flow in the last 10 min period was still 60% of that in the initial period. Amylase output was relatively high in the initial period but then declined more rapidly than the flow. The acini were densely packed with granules on the control side and showed a moderate amount of degranulation on the parasympathetically stimulated side. 3. After atropine (2 mg/kg I.V.), normal animals initially showed a moderate flow of saliva, being 41% of the non-atropinized animals, but there was a rapid decline and the total flow over 80 min was only 15% of that in the non-atropinized animals. The amylase secreted was also high initially and showed a rapid decline; the total amount secreted was similar to that in non-atropinized animals. The morphology was similar to that in non-atropinized animals and showed a similar loss of acinar granules on the stimulated side. 4. Chronic bilateral postganglionic sympathectomy (4-6 weeks duration) caused a drastic reduction in the capacity of the gland to secrete saliva in response to parasympathetic stimulation, reaching only one-third of that from normal animals. The initial output of amylase was greater than in normal animals but the total output was similar. The control unstimulated sympathectomized glands appeared similar morphologically to normal resting glands. However, on the parasympathetically stimulated side, besides the usual amount of acinar degranulation, there was also a conspicuous development of acinar vacuolation, not seen in the other groups of animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Amylases↗
PubMed2005

Bilateral thoracoscopic cervical sympathectomy for the treatment of recurrent polymorphic ventricular tachycardia.

Congenital long QT syndrome (LQTS) is a disorder of prolonged cardiac repolarisation, manifest by a prolonged QT interval and characterised by recurrent presyncope/syncope, polymorphic ventricular tachycardia (PMVT), or sudden cardiac death. A 46 year old woman with no family history of sudden death or deafness presented with recurrent syncope. Physical examination and electrolytes were normal and a 12 lead ECG showed a corrected QT interval of 458 ms. A monitored syncopal episode documented PMVT. Despite potassium and magnesium supplements, beta blockade, implantation of a single then dual chamber implantable cardioverter defibrillator (ICD), amiodarone, nicorandil, and mexiletine, the patient continued to experience arrhythmia storms, receiving more than 700 ICD discharges over seven months. She was ultimately treated successfully with bilateral thoracoscopic cervicothoracic sympathectomies. This is the first reported bilateral thoracoscopic treatment of a patient with LQTS and symptomatic life threatening ventricular tachyarrhythmias refractory to current pharmacological and pacing techniques.

Electrocardiography↗
PubMed1983

Chemical sympathectomy and serotonin inhibition reduce monocrotaline-induced right ventricular hypertrophy in rats.

Young male rats were administered monocrotaline (40 mg/kg, s.c.) either after chemical sympathectomy with 6-hydroxydopamine (6-OHDA, 100 mg/kg), after serotonin synthesis inhibition with p-chlorophenylalanine (PCPA, 500 mg/kg), or after saline injection. Monocrotaline rats exhibited a loss of body weight, marked right ventricular hypertrophy (RVH), increased pulmonary vascular muscularization, but no change in left ventricular weight or hematocrit at 20 days post-monocrotaline. Pretreatment with 6-OHDA or PCPA reduced the degree of RVH; however, neither 6-OHDA nor PCPA pretreatment prevented or reduced the pulmonary vascular muscularization associated with monocrotaline. Control, 6-OHDA-, and PCPA-treated rats exhibited only changes in ventricular weights associated with changes in their body growth. Thus, the sympathetic nervous system and serotonergic mechanisms seem to be involved in the development of monocrotaline-induced right ventricular hypertrophy, but are not responsible for the pulmonary vascular lesion.

Animals↗
PubMed1985

Acetylcholine supersensitivity in the rat heart produced by neonatal sympathectomy.

Effects of neonatal sympathectomy with antiserum to nerve growth factor or 6-hydroxydopamine on the acetylcholine sensitivity of the rat left atria were investigated. Sensitivities to acetylcholine of atria from immunologically and chemically sympathectomized rats were much higher than that of control at 4 weeks of age. These results suggest possible involvement of the sympathetic nervous system in regulation of cardiac cholinergic sensitivity.

Acetylcholine↗
PubMed1991

Effects of neonatal sympathectomy on brown fat development and susceptibility to high fat diet induced obesity in mice.

Injections of 6-hydroxydopamine in mouse neonates caused extensive and long lasting damage to the sympathetic nervous system and impaired brown fat development. Brown adipose tissue (BAT) thermogenic capacity of sympathectomized mice (up to 120 days old) was reduced because of marked reductions in the tissue mitochondrial protein content and the mitochondrial concentration of uncoupling protein, as assessed by [3H]GDP binding and immunoassay. Neonatal sympathectomy did not affect BAT DNA content. Sympathectomized mice also had reduced epinephrine-stimulated rates of oxygen consumption. BAT of sympathectomized mice failed to respond by increases in [3H]GDP binding to isolated mitochondria and uncoupling protein concentration when animals were offered a palatable high-fat dietary supplement that increased calorie intake of both normal and sympathectomized mice. The high-fat diet caused increases in body weight, carcass fat, and gonadal white fat pad weights in sympathectomized animals that were similar to those of control mice. These results show that inactivation of BAT metabolism did not accentuate the development of obesity caused by a dietary supplement rich in fat and suggest that stimulation of BAT metabolism was not very effective in counteracting the obesity-inducing effect of this diet.

Adipose Tissue, Brown↗
PubMed2002

Chemical sympathectomy alters regulation of body weight during prolonged ICV leptin infusion.

To assess the importance of the sympathetic nervous system in regulating body weight during prolonged leptin infusion, we evaluated food intake, body weight, and physical activity in conscious, unrestrained rats. Initial studies illustrated that prolonged intracerebroventricular (ICV) infusion of leptin enhanced substrate oxidation so that adipose tissue lipid stores were completely ablated, and muscle triglyceride and liver glycogen stores were depleted. After neonatal chemical sympathectomy, changes in weight and food intake were compared in groups of sympathectomized (SYM) and control (CON) adult animals during ICV infusion of leptin. CON animals lost 60 +/- 9 g over 10 days vs. 25 +/- 3 g in the SYM animals when food intake was matched between the two groups. Greater weight loss despite similar energy intake points to an important role of the sympathetic nervous system in stimulating energy expenditure during ICV leptin infusion by increasing the resting metabolic rate, since no differences in physical activity were observed between CON and SYM groups. In conclusion, activation of the SNS by leptin increases energy expenditure by augmenting the resting metabolic rate.

Adipose Tissue↗