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PubMed2001

Cardiac autonomic denervation and functional response to neurotoxins during acute experimental Chagas' disease in rats.

Severe cardiac autonomic denervation occurs in the acute Chagas' disease in rats. The present study aims at verifying whether this denervation was accompanied by impairment of heart function. Scorpionic (Tityus serrulatus) crude venom was used for neurotransmitter release in isolated hearts (Langendorff's preparation). In control hearts, the venom induced significant bradycardia followed by tachycardia. In infected animals, despite the severe (sympathetic) or moderate (parasympathetic) cardiac denervation, the venom provoked similar bradycardia but the tachycardia was higher. The hearts of infected animals beat at significantly lower rate. Atropine prevented this lower rate. Our results demonstrated sympathetic dysfunction during the acute phase of Trypanosoma cruzi infection in rats, the parasympathetic function being spared.

Acetylcholine↗
PubMed2000

Cardiac autonomic denervation in congestive heart failure: comparison of Chagas' heart disease with other dilated cardiomyopathy.

Congestive heart failure (CHF) is associated with activation of the cardiac sympathetic nerves. However, impairment of the sympathetic nerve terminals in patients with CHF has been indicated by studies showing reduction of cardiac norepinephrine uptake and stores. This investigation studies the histochemical evaluation of the sympathetic nerve terminals in CHF. The cardiac parasympathetic innervation was also studied to address the question of specificity of the presumed sympathetic denervation. Nineteen patients with CHF underwent cardiac transplantation or partial ventriculectomy, which provided the heart tissue. In 11 of them, the dilated cardiomyopathy was associated with Chagas' disease. Inflammatory process and fibrosis were studied histologically. The sympathetic and parasympathetic nerve fibers were visualized through histochemical techniques for, respectively, catecholamines and acetylcholinesterase activity. By using a computer-assisted morphometric program, the inflammation, fibrosis, and parasympathetic innervation were quantified. Moderate to severe fibrosing myocarditis characterized the hearts of the chagasic patients. In cardiomyopathies not associated with Chagas' disease, the inflammation was discrete, if present, but the amount of fibrosis was similar to that found in Chagas' cardiomyopathy. Reduction of both kinds of nerve terminals occurred in the heart of all patients. The parasympathetic denervation was proven to be more severe in chagasic cardiomyopathy. Our data on the heart innervation indicate a progressive autonomic denervation in heart failure. In Chagas' heart disease, the denervation seems to be more severe or rapid, probably because of the sustained inflammatory process.

Acetylcholinesterase↗
PubMed1990

Idiopathic autonomic denervation in eight patients presenting with functional gastrointestinal disease. A causal association?

Gut dysmotility may result from disease of the extrinsic neural pathways supplying the gut. We report the results of studies on sweating, cardiovascular, and sudomotor reflexes in eight prospectively evaluated patients with apparently functional gastrointestinal disorders. There was no personal or family history of neurologic disease, except for one patient with known atony of the bladder. Motility of the esophagus, stomach, and small intestine were, respectively, abnormal in two, six, and seven patients and showed either uncoordination of contractions between segments or postcibal hypomotility. All had generalized or patchy anhidrosis; quantitative sudomotor axon reflex tests were also abnormal in four patients and borderline in one. Plasma levels of catecholamines were abnormal in one patient. All patients had evidence of sympathetic denervation: preganglionic in two patients, postganglionic in five patients, and mixed in one patient. Three patients also had abnormal heart-rate responses to deep breathing, suggesting parasympathetic dysfunction. No underlying cause for the autonomic dysfunction was identified in any of these patients despite extensive investigations. Thus, these data support the hypothesis that apparently functional gastrointestinal disorders may be due to idiopathic autonomic denervation.

Adolescent↗
PubMed1998

Right ventricular infarction causes heterogeneous autonomic denervation of the viable peri-infarct area.

BACKGROUND: Because efferent autonomic pathways to the right ventricle (RV) differ from the efferent autonomic projections to the left ventricle (LV), we assessed the effects of RV infarction on this innervation. METHODS AND RESULTS: We measured the ventricular effective refractory period (ERP) shortening in response to bilateral ansae subclaviae stimulation and ERP lengthening induced by bilateral vagal stimulation as markers of autonomic innervation before and after RV myocardial infarction (RVMI) produced by coronary ligation (n=28 dogs) or intracoronary latex injection (n=18 dogs) into a marginal branch of the right coronary artery in open-chest anesthetized dogs. In each dog, ERPs measured in viable peri-infarct area at two RV outflow tract (RVOT) sites and two septal and four lateral sites at the RV free wall after RVMI showed reduced or absent ERP shortening during bilateral ansae subclaviae stimulation laterally, septally, and at RVOT sites 3 hours after RVMI. ERP shortening in response to infused norepinephrine was still present. Bilateral vagal stimulation during background norepinephrine infusion (0.10 to 0.25 microg/kg per minute) lengthened the ERP at all test sites before latex injection. After transmural RVMI, vagally induced ERP prolongation was attenuated or lost at lateral, septal, and RVOT test sites. CONCLUSIONS: RVMI causes sympathetic and vagal denervation at viable sites at the RVOT, lateral, and, to a lesser extent, septal sides of the viable peri-infarct area. Autonomic denervation in the RVOT might contribute to the development of ventricular tachyarrhythmias after the acute stage of myocardial infarction involving the RV.

Animals↗
PubMed1991

The effect of pinealectomy and autonomic denervation on crypt cell proliferation in the rat small intestine.

Previously it has been found that pinealectomy in rats was associated with increased small bowel crypt cell proliferation. The hypothalamus is thought to play a role in the neural control of crypt cell proliferation and the pineal gland is known to be functionally connected with this component of the autonomic nervous system. Consequently, the effect on crypt cell mitotic rate of pinealectomy with autonomic denervation of the rat small bowel (local sympathectomy and truncal vagotomy) was observed to determine the possible importance of the autonomic nervous system in the mediation of the effects of pinealectomy on the crypts. It was found that interruption of either the vagal or sympathetic nerve supply to the small intestine both significantly decreased the usual hyperproliferative effect on the crypt cells observed after pinealectomy. It is suggested that the overall effect of the pineal gland is to suppress the crypt cell proliferation rate and that this effect is mediated, at least to some extent, by (1) the direct connections between the pineal gland and the hypothalamus, (2) the connections between the hypothalamus and the vagal and sympathetic innervation of the gut, and (3) the influence of the autonomic innervation on the activity of the enteric plexuses in relationship to the crypts. The pineal may have a role in modulating the local control mechanism of crypt cell proliferation. Its exact role in the control of crypt cell proliferation has not yet been defined.

Animals↗
PubMed2000

[Autonomic nervous system and pancreas. (Analysis of the influence of different types of autonomic denervation in glandular regeneration phenomena and the interactions of the exocrine-endocrine-Axis)].

The present tests, in male Wistar rats, center around the trophic and functional changes of the pancreatic gland (R G), both exocrine and endocrine, induced by different types of autonomic nervous interruptions. First Group of Tests: Following one year celiac ganglionectomy (CG), nonpancreatectomized (Non-Pt) rats showed, basally, in blood, a drop of glucose (G), without changes of insulin (I). At autopsy, the CG animals showed an increase of the pancreatic we weight, of the total protein, of the RNA but not DNA. In the Pt. 95% rats, superimposing CG triggered, on the one hand, a drop to control values of the raised G blood levels, and on the other, a rise of I Besides, in feces, a rising of chymotrypsin concentration. At autopsy, in the PG, an increase of total protein and of RNA. Second Group of Tests: CG, after 6 months, induced, in blood, both basally and a 2 h glucose tolerance test, significant opposite enzyme activities changes in respect to C. Indeed, as amylase (A) was increased, that of lipase (L) was depressed. When alcohol feeding (AF) was superimposed to CG rats, a reversal of the L values was observed. The latter reached levels significantly higher those of the C. In in-vitro tests, the isolated islets of CG disclosed to release more I to the bath medium than those of the C animals. Third Group of Tests: Analyzing, in conscious animal, the L excretory changes in the basal bile pancreatic secretion (BB-PS) induced by chronic (2 months interruption of the autonomic nervous innervation of the PG, it was found that CG, truncal vagotomy (V), the association of CG + V, peri-Vaterian duodenotomy (PV-D), but not bilateral splachicectomy (Spl), inhibit, significantly the L output. It was also shown that superimosing AF to the V or CG + V animals reverted to C values the I depressed levels. In acute interruptions (24 h) of the autonomic nervous innervation of the PG: CG, V, P. V-D, the depression in the BBPS is highly significant, more than 40%. From these three sets of experiments it is concluded that: Firstly, CG increases the regenerative and functional capacity of both the exocrine pancreas. This is distinctively evident when the secretory mass is reduced like in the Pt. 95% series of animals. CG probably exerts its effects suppressing the releasing of some negative reins: adrenergic, pepdidergic (galanin). Secondly, CG evokes modifications of the normal Islet-pancreon inter-relationships. The rising of A and the drop of L in blood elicited by this type of autonomic nervous interruption probably reflects an increased release of I by the Langerhans islet. Thirdly, CG, the same as V. CG + V and P.V-D, but not Spl, depress the intrapancreatic cholinergic tone. This might by at the basis of the depression of L excretion in the BB-PS. The reversion to C Through the coupling of chronic alcohol intoxication to the autonomic decentralized PG would be a reflection of an increased sensitivity to ethanol of the intrapancreatic ganglionic neurons. The augmented acetylcholine release at the nerve terminal would lead to a high intrapancreatic cholinergic tone that, in the end, might be at the basis of the reversal changes induced in the autonomic decentralized PG by the chronic ethanol intoxication.

Animals↗
PubMed1991

Inhibition of activity-induced parotid growth by submandibular gland ablation or autonomic denervation.

When solid chow was reintroduced for 2 days to rats previously maintained on an all-liquid diet, [3H]thymidine incorporation into rat parotid gland was 2.4-4.4 times that of chow-fed or liquid-fed animals. When the submandibular-sublingual glands were removed before the change in diet from liquid to solid food, values for [3H]thymidine incorporation of parotid gland were not statistically different from those of chow-fed rats: the increase was completely prevented. The increase in gland size that accompanied the change in dietary consistency was not prevented by prior submandibular gland ablation; [3H]uridine incorporation was also not different from that of chow controls. The removal of both the sympathetic and parasympathetic nerves to the parotid gland before the dietary manipulation also suppressed [3H]thymidine incorporation into parotid, and values did not differ from chow controls. Moreover, the return to normal gland size (chow level) also was prevented by autonomic denervation. The data show an important role of the submandibular gland in regulation of the thymidine increase associated with the enhanced parotid activity that accompanies the change from liquid to solid diet. However, the submandibular gland does not have an important role in regulation of the increase in gland size that also accompanies the dietary change, whereas the autonomic nerves have an important role in regulation of hypertrophy and hyperplasia of parotid gland.

Animal Feed↗
PubMed1997

Correlation of the pilo-pupil ratio average, a new test for autonomic denervation, to the severity of diabetic retinopathy.

OBJECTIVE: To evaluate the association between the degree of diabetic retinopathy and autonomic neuropathy, and to test whether ocular parasympathetic denervation is correlated to the degree of diabetic retinopathy. DESIGN: Cross-sectional pilot study. SETTING: The tertiary ophthalmic centre for the Atlantic provinces in Halifax. PATIENTS: Twelve randomly selected patients (six women and six men with a mean age of 36.6 years) with insulin-dependent diabetes mellitus who had diabetic retinopathy. OUTCOME MEASURES: Degree of diabetic retinopathy, hemoglobin Alc level, orthostatic change in systolic and diastolic blood pressure and in serum catecholamine levels, degree of pupillary supersensitivity to 0.125% pilocarpine (pilo-pupil ratio average [PPRA]). RESULTS: The degree of diabetic retinopathy was significantly correlated with the duration of diabetes (p = 0.035), the hemoglobin Alc level (p = 0.004), the orthostatic change in diastolic blood pressure (p = 0.022) and the PPRA (p = 0.0007). CONCLUSIONS: The degree of diabetic retinopathy was significantly correlated with autonomic neuropathy and with the PPRA. Given these results, further study is indicated to determine whether autonomic neuropathy is a predictor of the severity of diabetic retinopathy.

Adult↗
PubMed2002

Effects of extrinsic autonomic denervation and myenteric plexus transection on colonic motility in conscious dogs.

BACKGROUND: The role of extrinsic autonomic nerves in regulation of colonic contractile activity is not well understood. METHODS: Twelve dogs had 6 strain gauge force transducers implanted in the colon and were divided into 3 experimental groups: (1) a control group, (2) an extrinsic denervation group (denervation group), and (3) an extrinsic denervation with proximal intrinsic myenteric plexus transection group (denervation + transection group). After recovery, colonic contractile activity during fasting and effects of feeding on gastrocolonic response were recorded. RESULTS: Colonic contractile activity occurred not only in the denervation group but also in the denervation + transection group. Both mean duration and propagation time of the colonic contractile activity were shorter in the denervation + transection group than in the control group. In the denervation group, propagation time was shorter than in the controls but the other parameters were not different. Feeding failed to immediately induce the gastrocolonic response in both experimental groups. CONCLUSIONS: We conclude that extrinsic nerves are not required for the appearance of colonic contractile activity. However, colonic contractile activity and its propagation are modulated by extrinsic innervation or proximal intrinsic neural continuity. Gastrocolonic response may be predominantly under extrinsic neural control.

Animals↗
PubMed2001

Pupillary autonomic denervation with increasing duration of diabetes mellitus.

BACKGROUND/AIMS: The autonomic pupillary changes in type I and II diabetic patients without clinical evidence of diabetic autonomic neuropathy (DAN) were compared with age matched controls. The relation between pupillary and cardiovascular autonomic function was assessed in the diabetic patients. METHODS: A case-control study was performed with diabetics grouped according to type and duration of diabetes. Static infrared pupillography was used to compare mean dark adapted pupil size and mean percentage changes in pupil size with pilocarpine 0.1% and cocaine 4% in the diabetic and control groups. All diabetic patients underwent cardiovascular autonomic function assessment using the Valsalva ratio, the 30:15 ratio, and testing for orthostatic hypotension. RESULTS: In total, 72 type I and 69 type II diabetic patients were compared with 120 controls. Mean dark adapted pupil size was significantly smaller in diabetic groups than controls. Except for type I diabetics with disease for less than 5 years, all patient groups had significantly greater mean percentage constriction in pupil size in response to dilute pilocarpine than controls. There was no significant difference between the mean percentage dilatation in response to cocaine 4% in diabetics and controls. A high proportion of patients had normal cardiovascular autonomic function particularly when this was assessed with the Valsalva ratio. CONCLUSIONS: Denervation hypersensitivity to dilute pilocarpine is a result of damage to the pupillary parasympathetic supply of diabetic patients. This occurs before the pupillary sympathetic pathway is affected, it can be detected early in the disease, and it may be a possible explanation for the small pupil size seen in diabetic patients. Pupillary autonomic dysfunction occurs before cardiovascular autonomic changes and detection of pupil denervation hypersensitivity to dilute pilocarpine is an inexpensive way to detect early DAN.

Adolescent↗
PubMed1983

Effect of autonomic denervation on DNA synthesis during liver regeneration after partial hepatectomy.

The regulatory role of autonomic nerves in liver regeneration after partial hepatectomy was studied in rats by bilateral subdiaphragmatic vagotomy or splanchnicectomy. 1. In control rats the wet weight of the regenerating liver was restored to approximately 80% of the preoperative weight 72 h after partial hepatectomy. Restoration of the liver weight was significantly impaired in vagotomy rats, but not in splanchnicectomy. Increases in the DNA and protein contents of the regenerating liver were also suppressed by vagotomy. 2. Hepatic DNA synthesis, measured as the incorporation of [methyl-3H]thymidine into DNA at various times after partial hepatectomy, was significantly less in vagotomized rats, and slightly more in splanchnicectomized rats than in control rats. The onset of DNA synthesis triggered by partial hepatectomy was also delayed by vagotomy. 3. The increases in activities of hepatic aspartate transcarbamoylase and thymidine kinase, the key enzymes in synthesis of pyrimidine nucleotides via the de novo and salvage pathways respectively, during liver regeneration, were significantly suppressed and retarded in vagotomized rats. Conversely, splanchnicectomy tended to stimulate these enzyme inductions after partial hepatectomy. 4. During starvation the plasma insulin level decreased after partial hapatectomy in control and vagotomized rats, as in sham-operated rats, but showed a transient increase 6 h after partial hepatectomy in splanchnicectomized rats. It is concluded that vagotomy inhibits and delays DNA synthesis and proliferation of liver cells after partial hepatectomy, whereas splanchnicectomy tends to stimulate these processes. The data also suggest that parasympathetic innervation of the liver may play an important regulatory role in liver regeneration.

Animals↗
PubMed1995

Reperfusion arrhythmias: role of early afterdepolarizations studied by monophasic action potential recordings in the intact canine heart during autonomically denervated and stimulated states.

INTRODUCTION: The precise mechanism of reperfusion arrhythmias is not established. The role of early afterdepolarizations (EADs) and triggered activity in the genesis of reperfusion ventricular arrhythmia was investigated. METHODS AND RESULTS: Monophasic action potentials (MAPs) were recorded in the canine heart using Ag-AgCl contact electrodes from the left and right ventricular endocardium and the left ventricular epicardial border zone during 10 minutes of occlusion of the proximal left anterior descending coronary artery followed by 2 minutes of reperfusion. Ventricular arrhythmias during ischemia and reperfusion were studied in three autonomically varied groups. Group 1 (n = 8) had intact autonomic neural innervation; group 2 (n = 8) had bilateral transection of ansae subclavii and vagi; and group 3 (n = 8) underwent bilateral transection of ansae subclavii and vagi with bilateral ansae subclavii stimulation during reperfusion. Ventricular fibrillation (VF) on reperfusion occurred in 2, 3, and 5 animals in the innervated, denervated, and sympathetically stimulated groups, respectively. Rapid ventricular tachycardia during ansae subclavii stimulation, antecedent to VF, occurred in 4 of 5 episodes in the sympathetically stimulated group. The frequency of premature ventricular complexes, couplets, and triplets on reperfusion was not significantly different among the three groups. Phase 2 or phase 3 EADs were noted during the acute ischemic phase in 6 of 8, 7 of 8, and 7 of 8 animals in the three groups, respectively (and persisted during reperfusion in the majority). Thus, these EADs were not a de novo phenomenon during reperfusion. Of the 72 MAP recording sites, only one demonstrated de novo phase 2 EADs during reperfusion. EADs disappeared during reperfusion in 6 animals (prior to the onset of VF in 4), and 5 dogs developed reperfusion VF without EADs being recorded. There was no direct correlation between the presence of EADs during reperfusion and the development of VF. The prevalence and onset of reperfusion VF was not significantly different in the presence of sympathetic stimulation. CONCLUSION: This study demonstrates that EADs can be recorded in the majority of dogs during both ischemia and reperfusion and do not appear to be a major mechanism responsible for reperfusion ventricular tachycardia and VF.

Action Potentials↗
PubMed1994

Reflex sympathetic dystrophy: result of autonomic denervation?

1. To investigate the nature of sympathetic dysfunction in the pathogenesis of reflex sympathetic dystrophy, the microcirculatory vasoconstrictive responses to dependency were investigated in the skin of the hand of 76 reflex sympathetic dystrophy patients with unilateral disease by means of laser Doppler flowmetry (in perfusion units) and capillary microscopy. The patients were divided into three stages according to their perception of skin temperature (stage I in the case of a stationary warmth sensation, stage II in the case of an intermittent warmth and cold sensation, and stage III in the case of a stationary cold sensation). The vasoconstrictive responses were induced by lowering of the affected hand. 2. As compared to controls, the mainly sympathetically mediated vasoconstrictive response at thermoregulatory level of the skin microcirculation, as measured by laser Doppler flowmetry, was attenuated at stage I (1.82 versus 1.41, P < 0.05), stage II (1.82 versus 1.09, P < 0.0001) and stage III (1.82 versus 1.14, P < 0.01), suggesting the involvement of sympathetic denervation at all stages of the reflex sympathetic dystrophy syndrome. This sympathetic denervation may also account for the observed increase in thermoregulatory skin blood flow at stage I as compared to controls (152 versus 81, P < 0.01). 3. Since sympathetic denervation has been reported to cause increased sensitivity of vascular structures to catecholamines, the decrease in thermoregulatory skin blood flow at stages II (54 versus 81, P < 0.05) and III (31 versus 81, P < 0.05), both as compared to controls, may result from hypersensitivity to catecholamines of skin microvessels. 4. The sympathetically independent vasoconstrictive response at the nutritive level of skin microcirculation, as measured by capillary microscopy, was impaired only at stage III as compared to controls (1.04 versus 2.06, P < 0.05). This divergence in microvascular reactivity upon dependency of the nutritive and thermoregulatory subsystems also supports the hypothesis of sympathetic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗