Autonomous denervation and salivary glands hypertrophy after parathyroidectomy.
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Animals↗
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Results for “Autonomic Denervation”
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Salivary CA130 with and without unilateral autonomic parotid denervation of rats fed different diets.
BACKGROUND: Tumor markers such as CA130 can be determined in human whole saliva. Saliva represents an attractive body fluid for longitudinal studies. MATERIALS AND METHODS: CA130 was determined in parotid saliva from 8 rats fed different diets, with or without autonomic denervation. RESULTS: CA130 could be determined in parotid saliva of rats, irrespective of diet and/or autonomic denervation. Whether the numerical decrease in CA130 observed after autonomic denervation is statistically significant requires further work. CONCLUSIONS: Since salivary CA130 has been shown to decrease following treatment with anti-cancer drugs in humans, the ability to determine this tumor marker in rat saliva opens new opportunities for optimizing cancer chronotherapy in the experimental laboratory.
Animals↗
[Advanced autonomic cardiovascular denervation of diabetic etiology. Presentation of a case].
"Functional" total cardiac denervation due to diabetic autonomic neuropathy, is relatively rare. Sympathetic and parasympathetic fibers differ in the frequency with which they are damaged, with preference of parasympathetic abnormality. We report a diabetic patient who presented cardiac denervation with fixed heart rate at rest (95 beats for minute), severe orthostatic hypotension and cardiovascular abnormalities such as absence of reactions to physiological and pharmacological stimuli, sympathetic and parasympathetic. To the best of our knowledge our patient is the third such case in the literature.
Autonomic Nervous System↗
The prevalence of autonomic neuropathy in insulin-dependent diabetes mellitus: a controlled study based on heart rate variability.
Autonomic function was investigated by tests of heart rate variation in 506 unselected insulin-dependent diabetics aged 12 to 85 years. Heart rate variability was measured by a computerised technique during rest and in response to a single deep breath, the Valsalva manoeuvre and standing. Changes in heart rate were compared with age-related normal ranges derived from 310 non-diabetic control subjects aged 18 to 87 years. Heart rate responses were found to be below the 5th centile control value in 13 to 23 per cent of diabetics. Impaired heart rate variability occurred more frequently in response to a single deep breath than to the other procedures. Results from all four procedures were combined in each subject to give an 'autonomic score', varying from 0 to 4. This score was greater than 1 in only five of 310 (1.6 per cent) non-diabetic control subjects. A score of 2 or more was therefore defined as abnormal and indicative of cardiac autonomic denervation. Abnormal autonomic scores were found in 84 diabetics (16.6 per cent). In diabetic subjects the autonomic score correlated most closely with heart rate variability at rest and in response to a single deep breath. Abnormal autonomic scores correlated significantly with duration of diabetes (p less than 0.0001) but not with age (p = 0.06). The frequency of abnormal autonomic scores was greatest in diabetics aged 40 to 49 years (24.5 per cent) and those with diabetes of 20 or more years duration (30.7 per cent).
Adult↗
Peripheral and cardiovascular autonomic impairment in chronic liver disease: prevalence and relation to hepatic function.
We have evaluated autonomic function using standard cardiovascular tests and a test of peripheral autonomic denervation, the acetylcholine sweatspot test, in 104 patients with biopsy proven chronic liver disease and 35 age- and sex-matched controls. Cardiovascular autonomic dysfunction was significantly more frequent in advanced liver disease compared with early liver disease (71.8% Child B or C vs. 39.7% Child A; p < 0.0006), and a strong correlation between the number of abnormal tests and Child-Pugh score could be demonstrated (Rs = 0.5; p < 0.0001). On multiple logistic regression analysis, cardiovascular autonomic dysfunction was related to age and to Child-Pugh score and occurred independently of the aetiology of liver disease. Peripheral autonomic denervation was found in 39% of patients, was significantly associated with cardiovascular abnormalities (p < 0.009) and correlated with the number of abnormal cardiovascular tests in each patient (Rs = 0.48; p < 0.0001). In chronic liver disease, the prevalence and severity of cardiovascular autonomic dysfunction is related to the severity of hepatic dysfunction and is independent of aetiology, suggesting a common pathogenetic basis related to hepatic damage; the association with peripheral autonomic denervation indicates that at least some of the abnormalities may be due to a true autonomic neuropathy. The possible significance of these findings to the complications of cirrhosis is discussed.
Acetylcholine↗
Quantitative effects of sympathetic and vagal nerve stimulations on sinus and AV junctional rhythms.
Responses of the sinus node and atrioventricular (AV) junctional pacemakers to autonomic denervation and to individual stimulations of the right and left stellate and both vagi were studied in 33 anesthetized dogs. Autonomic denervation depressed sinus node automaticity by only 18% from control, whilst AV junctional automaticity was reduced by 48.5% from control. Sympathetic and parasympathetic stimulation frequency-response curves (0.25, 0.5, 1, 2, 4, 8, 16 and 32 Hz) were obtained. In the sinus node the chronotropic responses to sympathetic stimulations reflect a bilaterally asymmetrical innervation with a right sided preponderance. In contrast, sinus slowing in response to either right or left vagal stimulations were indistinguishable when lower frequencies of stimulation were used. At 4 Hz and higher frequencies there is a right vagal preponderance. The AV junctional chronotropic responses suggest that this major subsidiary pacemaker receives a bilaterally symmetrical autonomic innervation. The chronotropic responses to individual nerve stimulations expressed as percent changes in sinus rate and AV junctional rate from their respective controls after autonomic denervation show that the AV junction is far more responsive than the sinus node to both sympathetic and parasympathetic stimulations. To allow for more meaningful comparisons the data were normalized using the respective maximum increase and maximum decrease of sinus node and AV junctional rates to left and right sympathetic and parasympathetic stimulations as the 100% reference. These normalized curves show that 50% of the maximal chronotropic responses were always achieved at a lower stimulus frequency in the AV junction than in the sinus node; shift of the AV junctional response curves to the left of the sinus node response curves by a 0.2 (sympathetic) and 0.3 (parasympathetic) log units was observed. These studies further showed that sympathetic activity in the AV junction is an absolute prerequisite to maintain regular AV junctional rhythms especially during the bradycardic episodes evoked in the study of vagal stimulus frequency-response curves.
Animals↗
Induction and recovery of colonic motility/defecatory disorders after extrinsic denervation of the colon and rectum in rats.
BACKGROUND: Anterior resection for rectal disease is associated with extrinsic autonomic denervation of the neorectum, which may influence the myenteric plexus, and subsequently the motility/defecatory status after operation. METHODS: A rat model with denervated neorectum was constructed. Colonic contractile activity in vivo, the amount of generic neuron marker (PGP 9.5) and nitric oxide synthase (NOS) were measured periodically. The responses of the muscle strip in each period to electrical field stimulation were evaluated using various neurotransmitters. RESULTS: In rats with denervated neorectum, giant migrating contractions (GMCs) of the distal colon, the number of fecal lumps per day and their small size, significantly increased in the early phase postoperatively, although both recovered in the late-phase period. The contractile response of the muscle strip of the denervated colon to acetylcholine was reduced throughout the period; however, contraction of the denervated colon under the addition of NO inhibitor (l-NAME) was enhanced significantly in the late-phase period, and recovered to the control level by atropine. Neuronal NOS, but not PGP 9.5 concentration, in the myenteric plexus at the distal denervated colon, significantly increased in the late-phase period. None of the above items differed from the control at other colonic portions throughout the period. CONCLUSIONS: Extrinsic autonomic denervation causes abnormal hyper-motility in the neorectum, which may be associated with multiple evacuations in the early phase postoperatively. Increased acetylcholine and the subsequent increase of neuronal NOS in the myenteric plexus may be an adaptive mechanism to compensate for such abnormal colonic motility after extrinsic denervation.
Animals↗
Effects of selective autonomic and pudendal denervation on the urethral function and development of retention in female dogs.
PURPOSE: This trial is an experimental approach to the possible causes of continence and voiding problems after urethra sparing radical cystectomy and orthotopic bladder substitution in women. MATERIALS AND METHODS: Between January 1996 and January 1999 we included 24 mongrel female dogs in this 4-phase study of 6 dogs each. The effects of autonomic denervation of the urethra (phase 1) and urethral transection just distal to the bladder neck (phase 2) on the urethral pressure profile were recorded. In phase 3 the effects of autonomic denervation, urethral transection and pharmacological manipulation of the denervated transected urethra on the urethral pressure profile were studied in succession. In phase 4 the effects of pudendal nerve transection and pharmacological blockade were recorded. In the 12 phases 2 and 3 dogs the transected urethra was re-anastomosed to the bladder neck. Acute experiments were repeated after 2 and 6 months, urethrocystoscopy was done and post-void residual urine was estimated. Two of the latter dogs were sacrificed 6 months after the acute experiment and the urethras were histopathologically examined. RESULTS: Autonomic denervation resulted in a 46% to 48% decrease in mean maximal pressure in the proximal urethra in phases 1 and 3 (p <0.001) with no significant effect on the distal urethra. Urethral transection in phase 2 did not affect the urethral pressure profile. Phentolamine injection after urethral denervation and transection in phase 3 produced a further reduction of 11.3% and 46.3% in mean resting pressure in the proximal and distal urethra, respectively, while succinyl choline produced a 38.1% further decrease in the distal urethra. Unilateral and bilateral pudendal denervation reduced pressure in the distal urethra significantly but not in the proximal urethra. When phentolamine was given thereafter, a further decrease of 38% and 2.4% resulted in resting pressure values in the proximal and distal urethra, respectively. The change in distal urethral pressure was marginally significant after succinyl choline injection (p = 0.05). Results were reproducible after 2 and 6 months. The proximal urethra remained patent with no post-void residual urine after autonomic denervation. There was no significant urethral fibrosis after realignment of the transected urethra in the 2 sacrificed phases 2 and 3 dogs. CONCLUSIONS: From this study we concluded that autonomic denervation reduced pressure in the proximal urethra by less than 50%. Continuity of the urethra with the bladder is not necessary for proper urethral function. After autonomic denervation the proximal urethra remained patent with no subsequent fibrosis. In addition, no post-void residual urine was noted. Bilateral pudendal denervation did not completely block activity of the distal urethra. The nonneuromuscular components had a small role in the creation of urethral closure function.
Animals↗
Influence of cardiac denervation on subsidiary atrial pacemaker stabilization.
Overdrive suppression was determined by measuring cardiac cycle lengths after rapid atrial pacing in nine alert conscious dogs sustaining total intrapericardial denervation. Rapid atrial pacing was performed at 125-400% of spontaneous heart rate for 30 s and at 200% spontaneous rate for 30, 60, 120, and 180 s, with and without cholinergic (atropine 0.2 mg/kg iv) or adrenergic blockade (propranolol 0.5 mg/kg iv). Corrected recovery time (CRT) was defined as the first recovery cycle length minus average control cycle length. To compare responses of the intact sinoatrial node (SAN) and subsidiary atrial pacemakers, CRT was measured in the conscious animal before and after SAN excision. Immediately after SAN excision, a junctional rhythm was frequently observed, but within a short time (min-h), subsidiary atrial pacemaker dominance was established with well-formed P waves and P-R interval averaging 85.3 +/- 3.4 ms. CRT before SAN excision ranged from 100 to 300 ms. Following pacing at 125-400% of spontaneous heart rate soon after SAN excision, CRT was markedly prolonged, ranging up to 6,000 ms. Atropine and propranolol did not influence CRT in the denervated preparation. CRT of subsidiary atrial pacemakers in the normally innervated dog heart returned to control pre-SAN excision values in 1-2 wk. In the denervated heart complete autonomic denervation exaggerated time required for return to control CRT values to 5-8 wk.
Animals↗
Functional alterations of the autonomic nervous system in Chagas' heart disease.
Several independent pathological studies in experimental models and in human beings showed conspicuous autonomic denervation in Chagas' disease. In spite of the inherently complex structural organization of the autonomic nervous system, the parasympathetic and sympathetic divisions are involved, as shown by many functional studies. Hence, Chagas' disease represents a unique model of impairment of the autonomic control of the heart, in absence of the nonspecific effects of cardiac failure. An improvement limitation of the studies thus far carried out is the lack of a better knowledge of the molecular biology characteristics of different strains of T. cruzi. This could explain some geographical discrepancies found in the clinical behaviour of Chagas' disease, and contribute to a better understanding of its pathophysiology.
Adult↗
Fear conditioning in humans: the influence of awareness and autonomic arousal on functional neuroanatomy.
The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal.
Aged↗
Calcific aortic stenosis and autonomic dysfunction.
With an aging population, calcific aortic stenosis is becoming more important in medical practice. Its cause is unknown. This paper hypothesises autonomic dysfunction is the abnormality underlying the tendency of the aging aortic valve to calcify, a proposition based on 2 main lines of evidence: 1. the similarity between aortic valvular calcification and medial arterial calcification, the latter a condition in whose pathogenesis autonomic dysfunction is implicated; 2. the similarity between the changes of autonomic denervation and those of natural aging in the aortic valve, of which calcific aortic stenosis is an exaggerated form. Autonomic denervation leads to withdrawal of neurotrophic influences from cells and tissues. The resulting changes in function and in structure, it is proposed, give rise to a condition of vulnerability allowing other stresses, such as haemodynamic trauma, to result in calcification.
Aged↗
Ocular autonomic nerve function in proliferative diabetic retinopathy.
Ocular autonomic nerve function was assessed in 28 diabetic patients with proliferative retinopathy (PDR) and 61 age- and sex-matched control subjects, by measurement of the pupil cycle time and determination of autonomic denervation hypersensitivity of the iris. Sustained pupil cycle time was absent in 88.5 per cent of PDR compared with 9.8 per cent of control subjects (p less than 0.001). Pupil constriction in response to 2.5 per cent methacholine--indicative of parasympathetic denervation hypersensitivity--was significantly increased in PDR (p less than 0.001), whilst pupil dilation in response to 0.5 per cent phenylephrine--indicative of sympathetic denervation hypersensitivity--was also significantly higher in PDR (p less than 0.001). Pupil reflexes were abnormal in 88.5 per cent of diabetics with proliferative retinopathy, with established autonomic denervation hypersensitivity in 57 per cent of patients.
Adult↗
[Effect of denervation following autonomic ganglia blockade on the work capacity of skeletal muscles].
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Animals↗
Topical apraclonidine testing discloses pupillary sympathetic denervation in diabetic patients.
BACKGROUND: Autonomic denervation is common in diabetes mellitus (DM). Pupillary sympathetic denervation (PSD) has been found in Horner syndrome following instillation of apraclonidine 0.5%. We have applied this technique to investigate the prevalence of PSD in DM. METHODS: Apraclonidine 0.5% was instilled in the eyes of 50 patients with DM and 30 age-matched and gender-matched subjects without DM (control subjects). Pupil diameters (PD) were measured before and 60 minutes after instillation. The duration of DM and the degree of diabetic retinopathy (DR) were recorded for each patient. RESULTS: Apraclonidine instillation caused an average of 0.9 mm of mydriasis (range 0 to 4.5 mm) in DM and -0.1 mm miosis (range 0.5 to -1 mm) in control subjects (P < 0.001). Mydriasis of at least 1 mm was observed in 42% of DM patients. The change in PD was highly correlated with the duration of DM (r = 0.368, P = 0.008) and the presence of DR (r = 0.532, P < 0.001). CONCLUSION: Apraclonidine testing, which is easy to perform and not distressing to the patient, identified PSD in nearly half of DM patients, the degree of mydriasis being correlated to the duration of DM and the presence of DR.
Administration, Topical↗
Case report: autonomic postganglionic denervation--sural nerve and saphenous vein biopsy.
The authors describe a 31-year-old woman of British Isle ancestry who developed a syndrome resembling familial dysautonomia in her early teenage years. Predominant manifestations included achalasia, severe orthostatic hypotension, and abnormal sweating. The study included resting and stimulated fractional catecholamines, which were almost nonexistent in both situations, and urinary catecholamines, demonstrating an increase in dopamine degradation products. Immunohistochemistry of saphenous vein was negative for dopamine beta-hydroxylase (DBH), serotonin (5-HT) and several vasoactive neuropeptides. The only neuropeptide detected at levels thought to be physiologically relevant was calcitonin gene-related peptide (CGRP), a vasodilator. This was in contrast to control veins, all of which had DBH and neuropeptide Y immunoreactive fibers but few CGRP fibers. Also in contrast to controls, electron microscopy of the saphenous vein indicated a close to total absence of terminals with norepinephrine containing vesicles. Sural nerve biopsy showed, on electron microscopy, a considerable reduction in the number of myelinated fibers, while unmyelinated fibers appeared to be in the normal range. The authors suggest, from the above findings, that the autonomic fibers were undergoing some form of distal axonal degeneration. Their findings differ from most biopsies performed in dysautonomic children, and they believe their patient has a different neurologic entity.
Adult↗
Heart rate variability in myocardial infarction with and without malignant arrhythmias: comparison with heart transplant recipients and normal subjects.
Myocardial autonomic denervation occurs after acute MI. This process is followed by a reduction of heart rate variability (HRV) and an increase of malignant ventricular arrhythmias and sudden death. This study investigated whether there are any significant differences in HRV among the population of MI who did and did not have malignant ventricular arrhythmias (MVAs), normal subjects and heart transplant recipients, the paradigm of the denervated heart. We studied 25 subjects aged 42 +/- 17 years, with normal clinical and cardiac noninvasive evaluation (group A); 70 patients aged 57 +/- 14 years, who had MI but no arrhythmic event in 36 months of follow-up (group B); 13 patients with MI aged 65 +/- 9 years, who had had sustained VT, VF, or sudden death (group C); and 16 cardiac transplant recipients aged 35 +/- 14 years (group D). The ECG was sampled for 256 seconds. We calculated, in time and frequency domain, the standard deviation of the RR cycle length and the spectral component's very low frequency (< 0.05 Hz), low frequency (0.05-0.15 Hz), and high frequency (0.15-0.35 Hz). The values of HRV in group A were significantly greater than in groups B, C, and D (P < 0.001) and greater in group B than in groups C and D (P < 0.001). Groups C and D did not differ (P = 0.610). These data indicate that HRV of patients who have had an MI and MVAs is very similar to that of heart transplant recipients. This is an indirect evidence that myocardial autonomic denervation may play an important role in the genesis of malignant arrhythmic events.
Adult↗
Rapid rates during bradycardia prolong ventricular refractoriness and facilitate ventricular tachycardia induction with cesium in dogs.
BACKGROUND: Bradycardia can promote the development of some ventricular techycardias (VTs). We investigated whether relative bradycardia per se or the transition from a rapid to a slower ventricular rate might be important in developing VT. METHODS AND RESULTS: We studied groups of anesthetized closed-chest dogs that had AV produced by radiofrequency catheter ablation of the AV junction. One group had uninterrupted AV block; the other group underwent a period of rapid left ventricular pacing. Both groups then received incremental doses of CsCl until sustained VT resulted. We also measured ventricular effective refractory period (V-ERP) and QT interval in separate groups of dogs that had AV block for 1 week or 3 days with and without rapid pacing (pacing cycle length [PCL] = 500 or 250 ms) for 1 hour or 30 minutes. Finally, we investigated the effects of rapid pacing on V-ERP by testing the effects of verapamil and autonomic denervation on these changes. We found that CsCl induced larger early afterdepolarizations and a greater prevalence of VT in dogs with rapid pacing than in dogs without. In dogs that had AV block for 1 week, 1 hour of rapid pacing prolonged V-ERP and QT interval compared with V-ERP and QT interval before pacing. Changes persisted for at least 3 hours. Rapid pacing for only 30 minutes and at a PCL of 250 ms, as well as superimposition on sinus rhythm, each prolonged V-ERP but to a lesser extent. Only 3 days of complete AV block and autonomic denervation did not affect the prolongation of V-ERP produced by rapid pacing, whereas verapamil significantly blunted but did not eliminate the prolongation. CONCLUSIONS: At the same PCLs, the heart exposed to transient tachycardia superimposed on bradycardia exhibited a longer V-ERP, QT interval, and monophasic action potential duration and greater ease for developing VT than the heart exposed only to bradycardia. The prolongation of refractoriness lasted for at least 3 hours, and the delta-ERP was influenced by the heart rate before pacing, the duration of pacing, and the PCL. The mechanism for this response to rapid rates appears to involve calcium, at least in part.
Animals↗