PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Autonomic Denervation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1997

Intrapericardial delivery of L-arginine reduces the increased severity of ventricular arrhythmias during sympathetic stimulation in dogs with acute coronary occlusion: nitric oxide modulates sympathetic effects on ventricular electrophysiological properties.

BACKGROUND: Nitric oxide (NO) modulates autonomic effects on myocardial contractility and sinus and atrioventricular nodal function of the heart. Whether NO influences autonomic actions on ventricular electrophysiological properties and arrhythmogenesis is not known. METHODS AND RESULTS: Four groups consisting of 43 autonomically denervated dogs were studied. To "superfuse" sympathetic nerves innervating the ventricles, test drugs were introduced into the pericardial sac for 30 minutes, and their effects on ventricular effective refractory period (ERP) and arrhythmia development were assessed before and during sympathetic stimulation (SS). In group 1 (n=12), ventricular ERPs showed no significant difference between control and superfusion with L-arginine, a NO precursor (222+/-20 versus 222+/-19 ms, P=.485). However, L-arginine significantly reduced SS-induced ERP shortening compared with control (9+/-7 versus 13+/-7 ms, P<.001). Simultaneous administration of N(G)-monomethyl-L-arginine (2 mg/mL) abolished the inhibitory effects of L-arginine (13+/-7 versus 13+/-7 ms, P=.885). In group 2 (n=15), the severity of ventricular arrhythmias significantly increased during SS. L-Arginine reduced this increase caused by SS. In group 3 (n=8), plasma norepinephrine spillover measured from the coronary sinus significantly increased during SS and was reduced by pericardial superfusion with L-arginine compared with control (6005.2+/-1525.6 versus 8503.4+/-2044.5 pg/min, P=.012). In group 4 (n=8), L-arginine pericardial superfusion significantly increased NO overflow measured from the coronary sinus during SS (93.25+/-59.20 versus 114.82+/-74.92 nmol/min, P=.043). CONCLUSIONS: Pericardial L-arginine reduces ERP shortening and increased severity of ischemic ventricular arrhythmias during SS in dogs. NO-induced reduction of norepinephrine release in the heart may be one of the underlying mechanisms.

Animals↗
PubMed1998

Reflex sympathetic dystrophy: facts and hypotheses.

Reflex sympathetic dystrophy (RSD) syndrome has been recognized clinically for many years. It is most often initiated by trauma to a nerve, neural plexus, or soft tissue. Diagnostic criteria are the presence of regional pain and other sensory changes following a noxious event. The pain is associated with changes in skin colour, skin temperature, abnormal sweating, oedema, and sometimes motor abnormalities. The clinical course is commonly divided into three stages: first (acute or hyperaemic), second (dystrophic or ischaemic), and third (atrophic) stage. The diagnosis is primarily clinical, but roentgenography, scintigraphy, thermography, electromyography and assessment of nerve conduction velocity can help to confirm the diagnosis. Although a wide variety of treatments have been recommended, the only therapies found to be effective in large studies aim at interfering with the activity of the sympathetic nervous system. To this end, efferent sympathetic nerve activity can be interrupted surgically or chemically. Alternatively, adrenoceptor blockers may be used to relieve pain. Numerous theories have been proposed to explain the pathophysiology. Sympathetic dysfunction, which often has been purported to play a pivotal role in RSD, has been suggested to consist of an increased rate of efferent sympathetic nerve impulses towards the involved extremity induced by increased afferent activity. However, the results of several experimental studies suggest that sympathetic dysfunction consists of supersensitivity to catecholamines induced by (partial) autonomic denervation. Besides, it has been suggested that excitation of sensory nerve fibres at axonal level causes release of neuropeptides at the peripheral endings of these fibres. These neuropeptides may induce vasodilation, increase vascular permeability, and excite surrounding sensory nerve fibres -- a phenomenon referred to as neurogenic inflammation. At the level of the central nervous system, it has been suggested that the increased input from peripheral nociceptors alters the central processing mechanisms.

Animals↗
PubMed2000

[Cardiac complications of type 2 diabetes].

Diabetic patients have a higher prevalence of hypertension, dyslipidemia and obesity. However, diabetes is by itself a major independent risk factor for cardiovascular disease. About two-thirds of total mortality are due to diabetic macroangiopathy. It is characterised by accelerated atherosclerosis, with more severe, more extensive and more diffuse lesions, as compared with nondiabetic patients. Patients with diabetes present more frequently acute pulmonary oedema despite similar infarct sizes than do nondiabetic patients. They are more frequently at risk for ventricular dysfunction, for ventricular aneurysm and for congestive heart failure. At the time of diagnosis of type 2 diabetes, more than 50% of patients have pre-existing coronary heart disease, probably related to painless ischemia, caused by an autonomic denervation of the heart in diabetic patients. International recommendations suggest that all diabetic patients should be evaluated at least annually for the development or progression of risk factors that would prompt cardiac testing. The standard bicycle exercise test should be chosen in an asymptomatic patient with only one other risk factor and with a normal resting ECG. For all other diabetic patients, stress echocardiography or stress myocardial perfusion imaging should be preferably chosen.

Cardiomyopathies↗
PubMed1979

Circulating antibodies to peripheral nerve in American trypanosomiasis (Chagas' disease).

An antibody reacting with Schwann sheaths of myelinated somatic and unmyelinated autonomic peripheral nerve was found in sixty-one out of seventy-one chronic, and nine out of ten acute, Chagas' disease sera. Indirect immunofluorescence (IFL) was carried out on rat, mouse and human somatic nerves and rat sympathetic nerves with initial serum dilutions of 1 : 10, and the staining reached a final titre of 1 : 320 in some cases. The antibodies fixed complement and were absorbed out by lyophilized epimastigotes of T. cruzi. Lipid extraction of the tissue sections enhanced the staining of myelinated nerve, whereas unfixed unmyelinated sympathetic nerve was strongly reactive. Central nervous tissue did not display any positive staining on neurons, glial cells or periaxonal sheaths. Furthermore, by using a double-labelled IFL technique, it was possible to show that a rabbit antiserum raised against guinea-pig spinal cord and the chagasic anti-nerve antibodies reacted with different structures in the rat sciatic nerve. These findings suggest that the reactive antigen(s) could be located on Schwann cells. The majority, but not all, of the chagasic individuals with anti-nerve antibodies also showed the sarcolemmal and endothelial staining (EVI) previously described in Chagas' disease. The possible recognition of Schwann cell antigens by circulating antibodies in Chagas' disease could be relevant, since an autonomic denervation has been postulated as a pathogenic mechanism of cardiomyopathy and megaviscera in this condition.

Animals↗
PubMedDate not supplied

[Physiology of the autonomic nervous system].

INTRODUCTION: The autonomic nervous system (ANS) is made up of a complex set of neurons and pathways that control the functioning of the different body systems within the organism. Its overall function is that of maintaining a state of homeostasis in the organism and of performing the adaptation responses when faced with changes in the external and internal environment. METHODS: The ANS is composed of visceral afferent pathways, integration centres at the brain stem, hypothalamus and cerebral cortex levels, as well as sympathetic and parasympathetic efferent pathways. The efferent pathways innerve the cardiac muscle, the smooth muscle and the exocrine and endocrine glands, while the afferent pathways are arranged in two patterns: oligosynaptic circuits, which mediate reflex adaptation responses of the visceral systems, and complex circuits, with projections to nuclei in the brain stem and the brain, where the information is collected and responses are produced that affect numerous systems. The afferent signals activate or inhibit the efferent components of the ANS by means of reflex pathways, independently of the will. These reflex circuits are also modulated by means of signals from central structures, and constitute a central autonomic neuronal network that integrates somatic, autonomic and affective responses. CONCLUSION: Dysfunctions of the ANS are possibly due to increases or decreases in autonomic control activity, which can appear because of lesions to the brain, spinal cord or peripheral nerves.

Autonomic Denervation↗
PubMed2003

Cardiovascular and pulmonary effects of epidural anaesthesia.

The cardiovascular effects observed with epidural anaesthesia are complex and are predominantly related to the extent of sympathetic denervation, autonomous balance, baseline blood volume and cardiovascular function of the patient. With epidural anaesthesia the pharmacological effect of systemically absorbed local anaesthetic agents and inclusion of adrenaline to the local anaesthetic solution may play a role. Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone prior to the block. Epidural anaesthesia per se has little effect on respiration in patients with pre-existing lung disease. Thoracic epidural anaesthesia appears to reverse the diaphragmatic dysfunction which is a major determinant of the decrease in lung volumes observed after upper abdominal surgery. This article summarizes cardiovascular and pulmonary responses to epidural anaesthesia.

Anesthesia, Epidural↗
PubMed1976

[Influence of reserpine on the nasal mucous membrane (author's transl)].

The influence of reserpine on the nasal mucous membrane in the various conditions of its autonomic denervation was investigated in the rabbits. Histochemical analysis of a acetylcholine esterase and quantitative measurements of acetylcholine were performed. The results point out that reserpine influence is found only on the vascular elements in the mucous membrane and not on the subepithelial glands. Analogically it was concluded that in some patients with arterial hypertension who were treated with reserpine, its side effect, nasal obstruction, was caused only by vasodilatation. In rhinitis vasomotorica, in the addition to the vasodilatation the abounding secretion of subepithelial mucous glands is present. The performed experiments also point out that resection of the vidian nerve in resistant cases of vasomotor rhinitis with aboundant secretion is reasonable.

Acetylcholinesterase↗
PubMedDate not supplied

Differences in left ventricular filling patterns in heart and heart-lung transplant recipients as assessed by Doppler echocardiography of transmitral flow.

The conventional surgical technique of orthotopic heart transplantation involves reconstruction of atria from donor and recipient components. The mechanical function of the atria is thus likely to be altered either by this anatomic disruption or by the autonomic denervation, which also occurs as a result of transplantation. We investigated 18 subjects with Doppler echocardiography of transmitral flow, to assess the contributions of passive and active filling of the left ventricle in six normal subjects, six heart transplant recipients, and six heart-lung transplant recipients. The ratio of passive transmitral flow to active flow was significantly higher in isolated heart transplant recipients than in normal subjects (p < 0.001), suggesting a reduced active, late diastolic component to left ventricular filling. This was not due to denervation, because the ratio in heart-lung recipients was lower than that in normal subjects (p < 0.01). These data suggest that anatomic rather than neural dysfunction is responsible for a major change in transmitral flow characteristics after isolated heart transplantation; whether the resulting change in pattern of left ventricular filling is clinically important deserves further investigation.

Blood Flow Velocity↗
PubMed2006

[Excitation and inhibition in monosynaptic reflex arcs of white rats in conditions of spinal hyperreflexia].

The mechanisms of excitation and inhibition in monosynaptic reflex arcs of white rats in conditions of spinal superreflexion (a state, in which the amplitude of reflex monosynaptic discharges of a ventral root (MD VR) is close to a threshold of excitation of motoneurons axon) were investigated. The character of MD VR during recording of their reflex discharges from cut and uncut VR was studied. Previously established pattern MR VR generation as extremely high voltage and presence of its second component are observed in these conditions. In a state of superreflexion intersegmental interactions getting weaker and are particularly characterized by inhibitive influences from segment L4 on motoneurons of segment L5. It is shown that in animals with spinal superreflexion expression of the antidromic inhibition is weaker compare to intact ones. It was defined that reciprocal interrelations of flexor and extensor motoneurons are maintained and even strengthen.

Animals↗
PubMed1989

Management of the diabetic foot.

Treatment of diabetic foot pathology requires an accurate assessment of the etiologic factors involved. Dysvascular deterioration may be amenable to vascular reconstruction. When the vascular status cannot be improved, however, amputation is preferable to continued conservative care. Neuropathic ulceration is the product of decreased sensation, deformity, and increased pressure at the site of the ulcer. Pressure relief by conservative or surgical means is required for healing. Neuroarthropathy is increasing in frequency and results primarily from autonomic denervation. Protection from weight bearing and orthotic control usually minimize deformity and ultimately restore the patient to an ambulatory status. Surgical intervention in neuroarthropathy may be effective when conservative means fail. All efforts at treatment may be undermined by poor compliance. Patient education, reinforced at each clinic visit, makes the patient a part of the treatment team.

Arthropathy, Neurogenic↗
PubMed1987

Trypanosoma cruzi (CL strain) infection in mice changes the chronotropic effect of isoproterenol in vitro.

Cardiac autonomic denervation has been reported to occur in experimental T. cruzi infection. We used isoproterenol (IP) to investigate the in vitro chronotropic sensitivity of atrial beta-adrenoceptors from mice acutely (30 days) or chronically (180 days) infected with T. cruzi, CL strain (a myotropic strain). Displacement of the dose-response curve to IP to the right occurred in the acute phase group. In the chronic phase group the opposite effect occurred (hyperreactivity to IP) although to a lesser extent. These results suggest that infection of mice with this strain of T. cruzi induces quantitative or qualitative changes in atrial beta-adrenoceptors.

Animals↗
PubMed1985

Appearance of the noradrenergic markers tyrosine hydroxylase and neuropeptide Y in cholinergic nerves of the iris following sympathectomy.

Selective autonomic denervations of the iris have been used to study the possible redistribution of adrenergic markers within adult nerve fiber systems and to reveal the cellular origin of a nonsympathetic fiber plexus induced to express such markers. The presence and distribution of fibers showing neuropeptide Y (NPY)- and tyrosine hydroxylase (TH)-like immunoreactivity was studied in the rat iris using stretch-prepared whole mounts. Normal irides contained a dense regular network of NPY-positive varicose fibers. Such fibers were regularly seen innervating blood vessels. The choroid membrane had a high number of fluorescent fibers. A similar, although slightly denser TH-positive fiber system was visualized in the iris. One or 2 days after surgical removal of the superior cervical ganglion, almost all NPY- and TH-positive fibers had disappeared, suggesting that most, if not all, NPY-positive fibers in the iris originate in the superior cervical ganglion. In irides from long-term sympathectomized animals, a high number of TH- and NPY-immunoreactive fibers had reappeared, while such irides were devoid of catecholamine-containing fibers, as evidenced by Falck-Hillarp histochemistry. The appearance of TH- and NPY-positive fibers in sympathetically denervated irides was clearly time dependent. The distribution of fluorescent fibers in irides from intact and sympathectomized animals showed obvious dissimilarities such as a lower fluorescence intensity and fewer varicose fibers in denervated irides. Furthermore, in irides from sympathectomized rats, TH- and NPY-positive fibers were not associated with blood vessels. Unilateral removal of the parasympathetic ciliary ganglion, which supplies the iris with cholinergic fibers, 3 days prior to sacrifice in animals bilaterally sympathectomized 1 month earlier, led to a drastic reduction in numbers of TH- and NPY-positive iris fibers on the ciliarectomized/sympathectomized side as compared to the sympathectomized-alone side. The present experiments thus suggest that adult cholinergic neurons in vivo are capable of expressing adrenergic characteristics under experimental conditions.

Adrenergic Fibers↗
PubMed1983

Sphincter of Oddi pressure in chagasic patients with megaesophagus.

Autonomic denervation is found throughout the entire length of the digestive tract in Chagas' disease. Anatomic evidence of myenteric ganglia reduction in chagasic gallbladders has been noted; however, the sphincter of Oddi has not been studied. The purpose of this study is twofold: first, to determine sphincter of Oddi pressure in 11 patients with chronic Chagas' disease and megaesophagus, and to compare the results with those obtained in 27 control subjects; and second, to evaluate the effect of cholecystokinin-octapeptide on sphincter of Oddi pressure in both groups of patients. Sphincter of Oddi pressure was recorded continuously via an endoscopically placed triple-lumen catheter inserted into the papilla and directed into the common bile duct. Basal sphincter of Oddi pressure was 12.9 +/- 1.1 mmHg in controls as compared with 44.9 +/- 4.7 mmHg in chagasics with megaesophagus. Mean common bile duct/duodenum gradient pressure was 4.1 +/- 2.4 mmHg in controls as compared with 13.1 +/- 2.7 mmHg in chagasics. Amplitude of sphincter of Oddi phasic contractions in the control group was 102.4 +/- 5.5 mmHg as compared with 140.5 +/- 9.2 mmHg in the chagasic group. Pulse dose of intravenous cholecystokinin-octapeptide produced a decrease of basal sphincter of Oddi pressure with inhibition of sphincter of Oddi phasic contractions in both chagasic and control patients. In chagasic patients, a neural abnormality in the sphincter of Oddi segment could explain the observed high basal pressure and high amplitude of phasic contractions. Chagasic patients with sphincter of Oddi pressure abnormalities, demonstrating sphincter of Oddi relaxation after cholecystokinin-octapeptide, may have neural impairment limited to preganglionic fibers, while the postganglionic inhibitory nerves remain at least partially intact.

Adolescent↗
PubMedDate not supplied

[Defecography in internal invagination of the rectum].

Rectal invagination has been considered an important cause of defecation difficulties and blockade (obstructed defecation). In the present study defecographies performed on 15 patients, with previous diagnosis of rectal invagination have been reviewed. Six patients had an intra-rectal (IR) invagination, three had an intra-anal (IA) invagination, while two patients did not show a typical rectal invagination. In the present series there is a suspected radiologic recurrence of the invagination. Three patients show a tendency to rectal stenosis. Anorectal angles at rest and under straining appears higher than the ones in normal subjects, after rectopexy, anorectal angles do not appear to be significantly changed and the pelvic floor is not significantly raising post-operatively. 7 out of 10 women had a rectocele preoperatively and 4 out 9 postoperatively. In 8 patients it was possible to compare a pre to a post-operative defecography. All patients but one displayed a reduction in the ability in emptying the rectum. The fact that rectal emptying is impaired may suggest that some autonomic denervation might occur following rectal mobilization.

Adult↗
PubMed1997

Histamine 2 receptor blocker-ranitidine and sinus node dysfunction.

BACKGROUND: Histamine 2 (H2) receptors were observed to be present in the sinus node. H2 receptor blockers could attenuate the histamine-induced increase in sinus rate and could thereby worsen sinus node dysfunction. However, the data pertaining to electrophysiological effects of H2 receptor blocker ranitidine on sinus node function are not available as yet, although bradycardia has been occasionally reported along with ranitidine. The present study evaluates the electrophysiological effects of ranitidine on sinus node function, and also determines the safety of administering ranitidine to patients suffering from sinus node dysfunction. METHODS: Thirty-nine patients with clinical diagnosis of sinus node dysfunction were selected for this study. Electrophysiological effects of intravenous injection of 150 mg ranitidine on sinus node function was evaluated. Tests were performed for 21 patients in the basal state (Group 1) and for 18 patients (Group 2) after autonomic blockade (propranolol 0.2 mg/kg, and atropine 0.04 mg/kg). The sinus cycle length (SCL), sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT), sinoatrial conduction time (SACT), atrio-His (AH) and His-ventricle (HV) intervals and blood pressure (BP) before and after ranitidine were analyzed. RESULTS: In Group 1, changes in SCL, SNRT, CSNRT, SACT, AH, HV and BP were not found to be significant. However, in Group 2, wherein the patients received ranitidine after autonomic blockade, it was observed that ranitidine significantly prolonged SCL (905.0 +/- 31.0 to 1000.0 +/- 40.0 msec, p = 0.001), decreased systolic BP (134.7 +/- 4.7 to 124.8 +/- 4.8 mmHg, p < 0.001), and diastolic BP (71.9 +/- 2.0 to 67.9 +/- 1.9 mmHg, p = 0.001), while the changes in SNRT, CSNRT, SACT, AH and HV were not significant. CONCLUSIONS: A clinical dose of 150 mg ranitidine must be administered by a slow intravenous infusion for at least 5 minutes in case of patients suffering from sinus node dysfunction. Continuous monitoring of BP and heart rate are necessary, especially in cases of autonomic denervation.

Adult↗
PubMed2001

Haemodynamics of the pressor effect of oral water in human sympathetic denervation due to autonomic failure.

Oral water ingestion increases blood pressure in normal elderly subjects and in patients suffering from autonomic failure, but the time course of the haemodynamic changes is not known. We therefore studied 14 subjects with documented sympathetic denervation due to pure autonomic failure, with continuous haemodynamic recordings obtained before and after ingestion of 500 ml of distilled water at room temperature. The time course of changes in values of systolic and diastolic beat-by-beat finger blood pressure, heart rate, stroke volume, cardiac output, ejection fraction and total peripheral resistance were analysed. Systolic blood pressure rose from 115+/-8 mmHg (mean+/-S.E.M.) to 133+/-8 mmHg (P<0.001), and diastolic blood pressure from 64+/-4 to 73+/-4 mmHg (P<0.001), with the pressor response beginning a few minutes after water ingestion, plateauing between 10 and 35 min (peak at 14 min), and returning to baseline at 50 min. Heart rate fell from 71+/-2.5 to 67+/-2 beats/min (P<0.001), and total peripheral resistance increased from 1.31+/-0.19 to 1.61+/-0.24 m-units (P<0.001). There were no significant changes in ejection fraction, stroke volume or cardiac output. This study confirmed a pressor response to oral water in subjects with sympathetic denervation. The temporal profile of the response did not favour reflexly mediated sympathetic activation. As subjects with autonomic failure are prone to salt and water depletion, and since blood pressure is exquisitely sensitive to such changes, it may be that the observed response is due to repletion or restoration of intravascular and extravascular fluid volume.

Adult↗