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At least 19 recordsLinked to original sources
PubMed1984

Fetal cardiovascular and catecholamine responses to hypoxemia after chemical sympathectomy.

Chemical sympathectomy was performed in fetal lambs in utero by daily intravenous administration of 6-hydroxydopamine (6HD) until a total dose of 60-70 mg/kg was reached. The completeness of adrenergic denervation was confirmed by the absence of any cardiovascular response to tryamine infusion. Baseline plasma catecholamine concentrations in normoxemic, sympathectomized fetuses were slightly higher than controls but the differences were not statistically significant. The concentration of norepinephrine (NE) was 313 +/- 73 pg/ml after 6HD administration compared with 259 +/- 25 pg/ml in control animals. Similarly, the concentration of epinephrine (E) was 39 +/- 15 pg/ml (6HD) versus 21 +/- 4 pg/ml (control). These mildly elevated catecholamine levels were accompanied by a small but significant increase in resting blood pressure (BP) (P less than 0.05). Heart rate (HR), however, was no different from control. Hypoxemia induced a marked increase in plasma catecholamines in control animals (NE, 2416 +/- 419 pg/ml and E, 2017 +/- 749 pg/ml) along with hypertension and bradycardia. Sympathectomized fetuses maintained a profound NE response to hypoxemia (NE, 1550 +/- 261 pg/ml) but a significant reduction in peak E response was observed (E, 244 +/- 42 pg/ml, P less than 0.05). HR and BP responses to hypoxemia were generally similar to control animals though there appeared to be a brief 1-3 min lag period between the nadir of the bradycardia and the peak of the BP response. We conclude that the generalized chemical sympathectomy after 6HD administration in the fetal lamb in utero is useful in evaluating the interaction of the autonomic nervous system and adrenal medullary function on the regulation of the fetal cardiovascular system.

Animals↗
PubMed1989

Sympathetic neural modulation of the immune system. I. Depression of T cell immunity in vivo and vitro following chemical sympathectomy.

Chemical sympathectomy of adult mice with 6-hydroxydopamine (6-OHDA) either prior to or following epicutaneous sensitization with the trinitrophenyl (TNP) hapten decreased the delayed hypersensitivity (DH) response to ear challenge. To determine if uptake of 6-OHDA into sympathetic nerve terminals, and their subsequent destruction, was required for suppression of DH, the catecholamine uptake blocker, desipramine, was employed to block 6-OHDA-induced sympathetic denervation. Pretreatment with desipramine prevented the depression of DH. In vivo treatment with the beta blocker, propranolol, did not alter the 6-OHDA effect, eliminating the potential contribution of released catecholamines, acting on beta-adrenoceptors, to DH reduction. Sympathectomy before sensitization also diminished hapten-specific T cell reactivity of sensitized lymph node (LN) cells, as measured in vitro by IL-2 production and CTL generation. In vivo DNA synthesis in draining LN in response to immunization was modestly decreased following 6-OHDA. Thus, sympathetic denervation appears to impair T cell activity in vivo and in vitro. Overall, these results indicate the SNS plays a role in generation of cell-mediated immunity.

Animals↗
PubMed1975

Radiology in chemical sympathectomy.

Chemical sympathectomy is an alternative to surgical sympathectomy when the patient's age or general condition precludes surgery. The indications and rationale in lower-limb arterial disease are discussed, and it is suggested that X-ray control is a valuable adjunct to the procedure.

Ganglia, Autonomic↗
PubMed2005

Aging and sympathetic modulation of immune function in Fischer 344 rats: effects of chemical sympathectomy on primary antibody response.

In aged Fischer 344 (F334) rats, sympathetic innervation of the spleen is markedly diminished compared with young rats. To determine if this diminished noradrenergic (NA) innervation maintains a functional connection with the immune system, 3- and 17-month-old male F344 rats were treated with the NA-selective neurotoxin, 6-hydroxydopamine (6-OHDA), to ablate peripheral NA nerve fibers. In sympathectomized rats immunized with keyhole limpet hemocyanin (KLH), a T-dependent protein antigen, anti-KLH IgM, IgG, IgG1, IgG2b antibody titers were increased in young and old rats 14 days after immunization compared to vehicle controls. Furthermore, the number of IgM and IgG anti-KLH antibody-secreting spleen cells was elevated 7 and 14 days post-immunization. These effects were prevented by pretreatment with desipramine, a catecholamine uptake blocker that blocks 6-OHDA uptake and subsequent sympathectomy. Chemical sympathectomy also increased KLH-induced proliferation in vitro by spleen cells from old, but not young animals. Isoproterenol (ISO), a beta-adrenergic receptor agonist, elicited a rise in cAMP in spleen cells from NA-intact young and old rats, but the increase was attenuated in spleen cells from old rats. These results demonstrate that, although NA innervation in the F344 rat spleen is diminished with age, sympathetic signaling of the immune system remains intact. Thus, the SNS can inhibit antibody produced in response to a protein antigen in both young and old F344 rats.

Adrenergic beta-Agonists↗
PubMed1988

[Receptor events after peripheral chemical sympathectomy].

Peripheral chemical sympathectomy by means of 6-hydroxydopamine does not influence the calorigenic effects of dobutamine, when given 3 days after 6-hydroxydopamine administration. After that time the sensitivity of the adrenoceptors, which are responsible for the calorigenic effects, did not increase.

Animals↗
PubMed1991

Neurogenic and non-neurogenic inflammation in the rat paw following chemical sympathectomy.

Rats with chemical sympathectomy, induced either at neonatal age (long-term sympathectomy) or in adult animals (short-term sympathectomy) by guanethidine or by 6-hydroxydopamine, were used to determine the contribution of sympathetic noradrenergic fibres to afferent neuron-mediated responses and to non-neurogenic inflammation in the rat. Following long-term sympathectomy with 6-hydroxydopamine there was a 66% depletion of noradrenaline in the paw skin. This was accompanied by a 20-53% increase in the levels of sensory neuropeptides in the paw skin and sciatic nerve. A hypersensitivity towards heat stimuli was observed in the tail immersion test. Neither neurogenic plasma protein extravasation following antidromic nerve stimulation or upon local mustard oil application nor the development of the non-neurogenic carrageenan oedema and its susceptibility towards indomethacin were impaired. Neonatal guanethidine sympathectomy caused an 86% depletion of noradrenaline in the paw skin and neurogenic plasma protein extravasation upon antidromic nerve stimulation was impaired. Sensory neuropeptides were unchanged in the skin after neonatal guanethidine and only calcitonin gene-related peptide content was increased in the spinal cord and sciatic nerves. The other observations (i.e. the sensitivity towards heat stimuli, the neurogenic mustard oil inflammation and the non-neurogenic carrageenan oedema) were similar to those observed after neonatal 6-hydroxydopamine treatment. Following the short-term treatment protocol of 6-hydroxydopamine, an 82% depletion of noradrenaline in the skin was accompanied by an increase in calcitonin gene-related peptide content, whereas after adult guanethidine (60% depletion of noradrenaline) levels of sensory neuropeptides were unchanged. Neurogenic plasma protein extravasation was found to be unimpaired after either type of short-term chemical sympathectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1987

Capsaicin-induced corneal lesions in mice and the effects of chemical sympathectomy.

Effects of chemical sympathectomy on corneal changes induced in mice by a s.c. injection of capsaicin were investigated. Pretreatment with a s.c. injection of 6-hydroxydopamine (6-OHDA) on the 1st and 2nd postnatal day or on the 14th and 15th postnatal day led to a marked suppression of the capsaicin-induced corneal lesions. This suppressive effect also was evident in case of administration after capsaicin treatment. Intraventricular injection of 6-OHDA had a slight, transient effect. DSP4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], another potent substance used for sympathetic denervation, had a suppressive effect similar to that of 6-OHDA. The concentration of capsaicin in tissues of the head was unaltered with 6-OHDA. The content of substance P (SP) in the ocular anterior segments was decreased, dose-dependently, with capsaicin administration. Neonatal administration of 6-OHDA decreased the rate of capsaicin-induced reduction of SP. However, this effect of 6-OHDA was too slight to explain the suppression of the corneal lesions, as the intensity score of lesions with a large dose of capsaicin after 6-OHDA was lower than that with a small dose of capsaicin without 6-OHDA, whereas SP content in the former was still much lower than that in the latter. On the other hand, the content of norepinephrine in the ocular tissues was decreased in the presence of 6-OHDA but not capsaicin. These results suggest that the corneal changes induced by capsaicin are largely inhibited by a decreased activity in the peripheral sympathetic system.

Animals↗
PubMed1985

Enhanced responsiveness of the coronary blood vessel of the dog heart-lung preparation to PGI2 after chronic chemical sympathectomy.

Chronic chemical denervation of the sympathetic nervous system with 6-OH dopamine resulted in an augmentation of the coronary blood flow (CBF) increase inherent in the canine heart-lung preparation, but not in an augmented accumulation of 6-keto PGF1 alpha in the circulating blood. In denervated HLP, 6-keto PGF1 alpha was lower and the vasodilator response to PGI2 larger at the start of the experiments. It was concluded that exaggerated increase in CBF was due to a potentiation of the vasodilator response to PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1997

Intracerebroventricular choline reverses hypotension induced by acute chemical sympathectomy.

1. The effect of centrally administered choline on blood pressure was investigated in rats made hypotensive by chemical sympathectomy. Chemical sympathectomy was produced by intravenous (i.v.) injection of 50 mg kg-1 of 6-hydroxydopamine (6-OHDA). Intracerebroventricular (i.c.v.) administration of choline (50-150 micrograms) 2 h after 6-OHDA treatment increased blood pressure and reversed the hypotension in a dose-dependent manner without affecting the heart rate. The pressor response was associated with an increase in plasma vasopressin levels. 2. Pretreatment of rats with the nicotinic receptor antagonist, mecamylamine (50 micrograms, i.c.v.), but not the muscarinic receptor antagonist atropine (10 micrograms, i.c.v.), blocked both the pressor and vasopressin responses to choline (150 micrograms). Pretreatment of rats with hemicholinium-3 (HC-3), a high affinity choline uptake inhibitor, greatly attenuated the pressor response to i.c.v. choline (150 micrograms). 3. The vasopressin V1 receptor antagonist, beta-mercapto-beta,beta-cyclopentamethylenepropionyl-O-Me-Try,Arg) - vasopressin (10 micrograms kg-1; i.v.) given 5 min after i.c.v. choline, decreased the blood pressure but failed to return it to the pre-choline levels. Prazosine (0.5 mg kg-1; i.p.), an antagonist of alpha-adrenoceptors, also decreased blood pressure. Administration of both antagonists together eliminated the pressor response to choline, and the blood pressure was reduced further to below the pre-choline levels. 4. It is concluded that i.c.v. choline can increase blood pressure in rats made hypotensive by acute chemical sympathectomy through the activation of central nicotinic receptors by presynaptic mechanisms. An elevation in plasma levels of both vasopressin and catecholamines (possibly released from the adrenal medulla) is involved in the pressor response to choline.

Adrenergic alpha-Antagonists↗
PubMed1986

A physiological basis for subclassifying beta-adrenoceptors examined by chemical sympathectomy of guinea-pigs.

Chemical sympathectomy of guinea-pigs was induced by chronic pretreatment with 6-hydroxydopamine over a 20 day period. Control animals were sham injected with vehicle at the same times. Isolated tissues were removed from the animals and beta-adrenoceptor sensitivity assessed from cumulative concentration-response curves for isoprenaline, followed after wash-out by a partial agonist (salbutamol, ritodrine or prenalterol). The following responses were measured: increases in force and rate of contraction of left and right atria respectively, inhibition of carbachol-induced ileal contractions, relaxation of intrinsic tone of lung strips and tracheal spirals, inhibition of contractions of vas deferens and soleus muscle induced by field stimulation. Left and right atria and ileum from 6-hydroxydopamine-pretreated guinea-pigs exhibited supersensitivity to beta-adrenoceptor stimulation. This was measured as a leftwards shift of the concentration-response curve for isoprenaline and as an elevation of the partial agonist maximum response (relative to isoprenaline), when compared with tissues from sham-injected controls. The supersensitivity was assumed to be due to the loss of endogenous neurotransmitter release by chemical sympathectomy and specific for the beta-adrenoceptor. In contrast, lung strips, vas deferens and soleus muscle were not supersensitive. The responses of these tissues are thought to be mediated via beta 2-adrenoceptors whereas cardiac and ileal responses are beta 1-adrenoceptor mediated. The latter receptor subtype would therefore appear to be under the influence of sympathetic innervation, but since no supersensitivity occurred at beta 2-adrenoceptors these were presumed to be non-innervated but stimulated by circulating adrenaline. These results obtained by use of chemical sympathectomy with 6-hydroxydopamine support the contention that the physiological basis of beta-adrenoceptor subclassification is that the beta 1-subtype are innervated whereas the beta 2-subtype are non-innervated.

Adrenergic beta-Agonists↗
PubMed1994

Sympathetic nervous system modulation of the immune system. II. Induction of lymphocyte proliferation and migration in vivo by chemical sympathectomy.

We have used chemical sympathectomy with 6-hydroxydopamine (6-OHDA) in adult mice to study the role of the sympathetic nervous system (SNS) in regulating cellular proliferation and migration in lymphoid organs. Following sympathectomy, an increase in inguinal and axillary lymph node (LN) weight and cellularity was observed. This increase paralleled increased cellular proliferation in vivo, as measured by uptake of [125I]deoxyuridine (125IUdR). Transient increases in cellular proliferation also were observed in spleen and bone marrow following sympathectomy. Administration of desipramine prior to 6-OHDA to prevent sympathectomy resulted in control levels of proliferation. beta-Adrenoceptor blockade just prior to or following 6-OHDA treatment did not alter the enhanced proliferation. Migration of normal 51Cr-labelled lymphocytes into inguinal and axillary LN was enhanced in sympathectomized recipients. Conversely, cells from sympathectomized animals showed diminished migration to these LN upon transfer into intact recipients. These results demonstrate that depletion of NA innervation alters cellular proliferation and lymphocyte migration in primary and secondary lymphoid organs.

Animals↗
PubMed1993

Morphometric evaluation of the rat testis, epididymis and vas deferens following chemical sympathectomy with guanethidine.

Selective chemical sympathectomy of the internal sex organs of adult male rats was undertaken by long term administration of low doses of guanethidine. The spermatogenic activity of the testis was unaffected by treatment. Examination of the vas deferens using morphometric methods revealed a marked increase in luminal area in contrast to a decrease in muscle layer area and in epithelial height. This is morphological evidence of sperm accumulation caused by a disorder in ductal contractile activity. No structural changes were observed in the epididymis. However, the concentration of spermatozoa in the sperm suspension stored in the cauda epididymidis was significantly increased in denervated rats. This result is discussed in terms of a sympathetic control of resorption mechanisms in the epididymis.

Animals↗
PubMed1990

Morphometric and biochemical evaluation of rat prostate and seminal vesicle following chemical sympathectomy with guanethidine.

Selective chemical sympathectomy of the internal genital organs of adult male rats was undertaken by chronic treatment with low doses of guanethidine. Biochemical and morphometric methods revealed that removal of sympathetic innervation prevents fructose secretion in the prostate and seminal vesicle, in addition to promoting reduced efficiency of delivery by the latter.

Animals↗
PubMed1988

[Study of species differences on chemical sympathectomy: rats and guinea pigs].

Chemical sympathectomy induced by guanethidine or 6-hydroxydopamine (6-OHDA) and reserpinization were investigated by their influences on the cardiovascular system in urethane-anesthetized rats and guinea pigs and on nerve endings in the atrium or aorta and adrenaline-containing granules in the adrenal medulla. In rats, guanethidine and 6-OHDA significantly lowered the basal blood pressure, but reserpine did not. In guinea pigs, none of them affected the basal blood pressure, and with the exception of the potentiation of adrenaline-induced pressor responses, the influences of all 3 drugs on adrenaline- and tyramine-induced responses in blood pressure and heart rate were weaker than those in rats, but influences of treatments with guanethidine for 1 week were more striking than those for 5 weeks. There were significant differences between rats and guinea pigs in classified forms of nerve endings in the right atrium and of adrenaline-containing granules in the adrenal medulla or differences in the influences on the adrenal medulla by all 3 drugs. Only 6-OHDA induced injury in rat atrium. The above results suggest that there are species differences between rats and guinea pigs, not only in the chemical sympathectomized animals but also in the normal condition and that the pharmacodynamic effect of chemical sympathectomy is more prominent in rats than in guinea pigs.

Adrenal Medulla↗
PubMed1989

Monoamine oxidase (MAO) in pancreatic islets of the mouse: some characteristics and the effect of chemical sympathectomy.

We have previously observed that chemical sympathectomy in the guinea pig induced an increase in the intensity of serotonin fluorescence in the insulin cells of the pancreatic islets. In the present study we have studied some basal characteristics of mouse islet monoamine oxidase (MAO) and the effect of chemical sympathectomy induced by 6-hydroxydopamine on the activity of this enzyme. Estimated Km-values for MAO activity with different substrates were as follows: serotonin (5-HT; 2 x 10(-4) M), dopamine (DA; 4 x 10(-4) M), and 2-phenylethylamine (PEA; 4 x 10(-6) M). The highest specific activity was displayed with PEA and DA as substrates, whereas it was about 10 times lower with 5-HT as substrate. Two days after the destruction of islet adrenergic nerves by 6-hydroxydopamine we observed a decrease of approximately 30% of the MAO activity with serotonin as substrate and after seven days the MAO activity with PEA as substrate had decreased by 18%. By contrast the MAO activity with DA as substrate was slightly increased (+ 12%) at two days after sympathectomy. There is a need for a further characterization of islet MAO activity(ies) and for further studies on its putative role in insulin secretory processes through its regulation of the islet monoamine stores.

Animals↗
PubMed2001

The effects of chemical sympathectomy on testicular injury in varicocele.

OBJECTIVE: To determine whether the sympathetic nervous system plays a role in the contralateral testicular deterioration encountered in varicocele. MATERIALS AND METHODS: Forty male Sprague-Dawley albino rats (28 days old) were divided equally into four treatment groups, i.e. (1) sham operation, (2) with varicocele, (3) treated by chemical sympathectomy plus varicocele, and (4) chemical sympathectomy only. Chemical sympathectomy was induced by administering intraperitoneal 6-OH dopamine (100 microg/g for 5 days) in groups 3 and 4; groups 1 and 2 received equal volumes of physiological saline by the same route. All rats underwent laparotomy and part of the left renal vein (distal to the spermatic vein confluence) was isolated and encircled with a 4/0 silk suture. The suture was left untied in group 2, and tied around a 24 F peripheral venous cannula in groups 3 and 4. The testes were then excised when the rats were 70 days old; malondialdehyde (MDA) in the testicular tissue was assayed by the thiobarbituric acid-reactive substances method, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels were determined by spectrophotometric analysis. RESULTS: Varicocele resulted in a significant increase in MDA levels in both testes and chemical sympathectomy prevented this effect. SOD and GSH-Px values were significantly decreased in both testes in group 2; chemical sympathectomy also prevented this effect. CONCLUSION: An induced unilateral varicocele significantly increases the biochemical indicators of tissue hypoxia in both testes. As this increase was prevented by chemical sympathectomy, the sympathetic nervous system may play a role in the testicular degeneration associated with varicocele.

Animals↗