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Diastolic dysfunction and autonomic abnormalities in patients with systolic heart failure.

BACKGROUND: Patients with systolic heart failure (SHF) often have concomitant diastolic dysfunction (DD). SHF is associated with decreased heart rate variability (HRV), but the impact of degree of DD on HRV in SHF is unclear. METHODS AND RESULTS: HRV was measured in 139 patients, aged 64+/-12 years, 74% male, LVEF 30+/-8%. Patients had stable NYHA class II-III CHF on ACE inhibitors or ATII receptor blockers, with LVEF or=200 pg/ml. Subjects underwent 2-D echocardiography with Doppler assessment and 24-h Holters. Patients were categorized as having impaired relaxation (E-deceleration time>2 SD above age-adjusted normal values (AANV), E/A or=1; N=30), pseudonormal (E-deceleration time within 2 SD of AANV, E/A=1-2, systolic/diastolic pulmonary vein flow<1; N=25) or restrictive filling patterns (E-deceleration time>2 SD below AANV or/and E/A ratio>or=2; N=84) Differences were adjusted for clinical covariates using UNIANOVA, p<0.05. HRV was reduced and BNP higher in pseudonormal patients compared to impaired relaxation, but this difference was only significant for restrictive vs. impaired filling. Differences remained significant after adjustment for covariates. CONCLUSION: Significantly more abnormal HRV, reflecting greater cardiac autonomic dysfunction, is associated with restrictive DD compared to impaired relaxation.

Adult↗

QT dispersion and autonomic nervous system function in patients with type 1 diabetes.

Cardiac arrhythmias and markedly increased mortality rate have been demonstrated in patients with diabetic autonomic neuropathy. Abnormal prolonged QT dispersion interval (QTd) is associated with a higher risk of ventricular arrhythmias. The aim of this study was to evaluate the relationship between autonomic dysfunction, QT and JT interval dispersion parameters and ventricular arrhythmias. Twenty-six patients with type 1 diabetes mellitus and 20 healthy subjects as controls were enrolled in the study. Resting 12-lead electrocardiograms were recorded for measurement of QTd, corrected QTd (QTcd), JT dispersion (JTd) and corrected JT dispersion (JTcd). After taking ECG, all patients underwent autonomic function tests. Patients and control group were also evaluated by 24-h Holter monitoring. Fourteen patients were identified who had autonomic dysfunction. QTd, QTcd, JTd, and JTcd values were significantly higher in patients with autonomic dysfunction than both patients without autonomic dysfunction and the control group (QTd: 78+/-16 vs. 51+/-13 ms, P=0.002; 78+/-16 vs. 48+/-9 ms, P<0.001; QTcd: 91+/-14 vs. 66+/-12 ms, P=0.001; 91+/-14 vs. 61+/-11 ms, P<0.001; JTd: 81+/-12 vs. 58+/-13 ms, P=0.001; 81+/-12 vs. 49+/-7, P<0.001; JTcd: 96+/-15 vs. 73+/-11 ms, P<0.001; 96+/-15 vs. 67+/-8 ms, P=0.001). There was no significant difference between the dispersion parameters in diabetic patients without autonomic dysfunction and the control subjects (P>0.05). Also, patients with autonomic dysfunction had higher Lown classes of ventricular arrhythmias and patients with higher Lown classes of ventricular arrhythmias had more prolonged QTd and QTcd values. The data suggest that diabetic patients with autonomic dysfunction have increased dispersion of ventricular refractoriness, which may be one of the factors contributing to the increased incidence of arrhythmias and sudden death observed in these patients.

Adolescent↗

Autonomic nerve dysfunction is closely associated with the abnormalities of esophageal motility in reflux esophagitis.

BACKGROUND: While reflux esophagitis (RE) is often associated with esophageal motility dysfunction, the causes of this abnormal motility are not well understood. The aim of our study was to assess the relationship between esophageal motility and autonomic nerve dysfunction by comparing 14 healthy control subjects (11 M, 3 F; mean age, 56.4 years) with 26 patients with RE (19 M, 7 F; mean age, 60.4 years). METHODS: According to results of esophageal manometry, subjects with RE were assigned to group I (RE with esophageal motility dysfunction, n = 12) or group N (RE without motility dysfunction, n = 14). Autonomic neuropathy was assessed by measuring the heart rate coefficient of variation at rest (CVR-R), the Valsalva ratio for the R-R interval, the systolic blood pressure response to mental calculation, and the antral contractile response to modified sham feeding (MSF). RESULTS: CVR-R at rest was lower in group I (2.08 +/- 0.18) than in group N (3.80 +/- 0.44; P < 0.05). The frequency of antral contractile response to MSF per 3-min interval over 15 min was significantly lower in group I than in either group N or controls. The 15-min integrated antral contractile response, taken as the area under the contraction time curve, was much lower in group I (13.2 +/- 6.2) than in controls (55.6 +/- 9.2; P < 0.01). CONCLUSIONS: We conclude that esophageal motor dysfunction in some patients with RE may result from autonomic dysfunction.

Adult↗

Cardiovascular autonomic nerve function in patients with hypoxaemic chronic obstructive pulmonary disease.

Intraneural hypoxaemia is recognized as a pathogenic mechanism in diabetic neuropathy. A similar pathophysiological process may occur in chronic obstructive pulmonary disease (COPD). Autonomic neuropathy is not recognized in COPD. We compared 96 patients with hypoxaemic COPD to 22 age-matched control subjects to see whether autonomic dysfunction occurs in COPD and whether there was any correlation with the severity of hypoxaemia. The cardiovascular autonomic tests consisted of heart rate responses (mainly parasympathetic function) to a Valsalva manoeuvre, deep breathing and postural change and blood pressure responses (mainly of sympathetic origin) to postural change and sustained handgrip. Early autonomic neuropathy is defined as one abnormal test and definite autonomic neuropathy as two abnormal tests according to the normal range. These autonomic tests were reproducible in our study population. Although the symptoms and signs of autonomic neuropathy were rare, definite autonomic dysfunction was found in 35%, and early autonomic neuropathy in a further 47%, of patients whose arterial oxygen tension (PaO2) was less than 8 kPa (60 mmHg). Only 18% of the control group had evidence of an age-related early autonomic dysfunction. Parasympathetic autonomic dysfunction was significantly correlated with PaO2 whilst the sympathetic tests were relatively normal. Correction of hypoxaemia for one hour or administration of ipratropium bromide or terbutaline had no effect on autonomic function. Subclinical autonomic neuropathy is a feature of hypoxaemic COPD. Its importance in the disease process and its role in prognosis needs evaluation.

Aged↗

Influence of orthostatic hypotension in Parkinson's disease on plasma atrial natriuretic peptide.

The effect of orthostatic hypotension in Parkinson's disease (PD) on plasma atrial natriuretic peptide (ANP) was examined in fifteen individuals with PD without autonomic dysfunction (63-85 years), nine PD patients with autonomic dysfunction (orthostatic hypotension; systolic BP change > 20 mmHg after 5 min standing: 69-82 years) and 14 fit elderly volunteers (62-93 years). The mean ANP level was 42.2 pg/ml (range 16.8-89.2 pg/ml) in the PD group without autonomic dysfunction; 44.4 pg/ml (range 27.2-91.2 pg/ml) in the PD group with autonomic dysfunction; and 48.5 pg/ml (range 22.2-111.6 pg/ml) in the elderly group. There was no statistical difference in plasma atrial natriuretic peptide between all three groups. The mean change in blood pressure was -39 mmHg (systolic) and -18 mmHg (diastolic) between supine and standing in the group with orthostatic hypotension.

Journal Article↗

Autonomic nerve dysfunction in systemic lupus erythematosus: evidence for a mild involvement.

Neurologic manifestations are known to occur in patients with systemic lupus erythematosus (SLE) and significantly affect the clinical course of the disease. Nevertheless, the prevalence, pattern and severity of autonomic impairment in such patients have yet to be defined. In the present study a series of 38 female SLE patients was assessed for the presence of autonomic dysfunction. Five noninvasive standardized cardiovascular reflex tests were used. The grading system proposed by Ewing and Clarke was applied to classifying autonomic impairment according to severity. Seventeen out of 38 patients, that is 44.7%, had evidence of autonomic impairment. Most of the patients had a mild degree of dysfunction. No correlation was found for the duration of the disease while an apparent lack of the commonly described chronological sequence of autonomic involvement was observed. We suggest that in SLE patients the prevalence of autonomic impairment, when investigated, does not significantly differ from that of other SLE-associated neurological events. The contribution of a direct immunological damage to components of neural pathways in the pathogenesis of the autonomic involvement can be postulated. Clinical consequences of autonomic impairment in patients with systemic lupus erythematosus need to be elucidated.

Adaptation, Physiological↗

Autonomic nerve dysfunction in COPD as assessed by the acetylcholine sweat-spot test.

Patients with hypoxic chronic obstructive pulmonary disease (COPD) have evidence of a subclinical parasympathetic autonomic neuropathy, with apparent preservation of sympathetic function. However, these cardiovascular-respiratory tests might have been biased by concomitant chest disease, the acetylcholine sweat-spot test avoids this bias. This sweat-spot test assesses sympathetic nerve function, it relies upon the fact that denervated sweat glands do not produce sweat. 35 patients with hypoxaemic COPD and seven age matched normal subjects were studied. Following intradermal injection of 0.1 of 1% acetylcholine into the dorsum of the feet, the number of sweatglands able to respond in a given surface area was recorded. Cardiovascular autonomic nerve function, arterial oxygen and carbon dioxide tensions, lung function and cigarette consumption were also recorded. The acetylcholine sweat-spot test was highly repeatable in eight COPD patients, no person with normal or frankly abnormal function being wrongly assigned. The age matched control subjects had normal acetylcholine sweat-spot scores and cardiovascular autonomic tests. The acetylcholine sweat-spot test was abnormal in 24 patients, borderline in 8 and normal in 3 patients. The abnormal sweat-spot test group had significant worse FEV1, arterial blood gases and autonomic function. The acetylcholine sweat-spot score correlated with the severity of arterial hypoxaemia (r = 0.78, p < 0.001) and with the parasympathetic cardiovascular tests (r = 0.80, p < 0.001). In conclusion, patients with hypoxaemic COPD have a parasympathetic cardiovascular and a peripheral sympathetic autonomic neuropathy. The acetylcholine sweat-spot test is repeatable, easy to perform and a sensitive indicator for autonomic dysfunction in breathless individuals with COPD.

Acetylcholine↗

[Gastrointestinal motility and autonomic nerve dysfunction].

Gastrointestinal motility is greatly influenced by both the autonomic nervous system (ANS) and the enteric nervous system (ENS). Dysfunction of ANS and/or ENS produces various kinds of dysmotility from the esophagus to the colon. Generalized autonomic dysfunction, often seen in diabetics, causes abnormal peristaltic waves in the esophagus, abnormal electrical activity of the stomach, delayed gastric emptying and delayed intestinal transit. Localized disorders of the enteric nervous system is seen in patients with achalasia and Hirschsprung's diseases. Functional disorders, without evidence of organic disorders, like non-cardiac chest pain, non-ulcer dyspepsia, irritable bowel syndrome, can be partly caused by abnormal function of autonomic nervous system.

Autonomic Nervous System↗

Autonomic nervous dysfunction in severe pre-eclampsia.

We evaluated autonomic nervous function in 14 subjects with severe pre-eclampsia and 11 subjects with normal third-trimester pregnancies using standard cardiovascular tests, i.e. heart rate responses to deep breathing and standing up, and blood pressure response to standing up. Both of the heart rate responses were lower in subjects with severe pre-eclampsia than in the control group (P less than 0.01 and P less than 0.001, respectively). Four subjects with severe pre-eclampsia had postural hypotension, defined as a systolic blood pressure fall of at least 30 mmHg on standing. Our results show that severe pre-eclampsia may be associated with autonomic nervous dysfunction. The inability to regulate heart rate and blood pressure in response to postural alterations may compromise the placental and renal blood flow in certain conditions, emphasising the importance of bed rest in severe pre-eclampsia.

Adolescent↗

Characterization and natural course of cardiac autonomic nervous dysfunction in HIV-infected patients.

OBJECTIVE: To examine the degree, pattern, and natural history of cardiac autonomic nervous dysfunction in patients infected with HIV. DESIGN: Cross-sectional and prospective longitudinal cohort study. SETTING: Primary care and tertiary referral university centre. PARTICIPANTS: Thirty-five consecutive HIV-infected patients who had either not yet developed AIDS (15 pre-AIDS patients) or who were at the Centers for Disease Control and Prevention (CDC) AIDS stage (n = 20), and 29 healthy age- and sex-matched HIV-negative controls. METHODS: Computer-aided power spectral analysis of 15 standardized parameters of heart-rate variability (HRV). RESULTS: Pre-AIDS patients as a group did not exhibit any HRV parameters to be significantly different from healthy controls (P > 0.017), whereas AIDS patients demonstrated reduced HRV in 14 parameters (93.3%) compared with healthy subjects (p > 0.017). Median proportion of abnormal HRV parameters (< 10th percentile of controls) per individual was 9.1% in pre-AIDS patients and 61.3% in AIDS patients (P = 0.0347). Progressive CDC stages inversely correlated to 10 HRV parameters (66.7%; -0.50 < or = r < or = -0.36; P < 0.05). Follow-up testing in 10 pre-AIDS and six AIDS patients after 6-16 months (median, 12.5 months) did not reveal deterioration of HRV (P < 0.05). A dysautonomia symptom score correlated to 10 HRV parameters (66.7%; -0.14 < r < -0.55; P < 0.05). CONCLUSIONS: Cardiac autonomic nervous dysfunction is severe in AIDS patients, although not significant in pre-AIDS patients. Cardiac autonomic nervous dysfunction proceeds with HIV disease progression, although its individual course is slow.

Adolescent↗

[Sudomotor dysfunction in Parkinson's disease].

Autonomic dysfunction is often associated with the progression of Parkinson's disease (PD). The most frequent manifestations of autonomic dysfunction are cardiovascular symptoms, bladder and bowel dysfunction, and sudomotor dysfunction. However, sudomotor dysfunction in PD remains poorly understood. To evaluate sudomotor function in PD, we quantitatively measured sweating during untreated conditions in 20 patients with PD (age, 62 +/- 5 years) and in 10 age-matched control subjects (60 +/- 6 years). An evaporimeter can measure small amounts of water (g/m2h) evaporated from the body. This device was used to quantify sweating at different sites of the skin (forehead, arm, dorsal part of hand, chest wall, femur, and dorsal part of foot). Sweating demonstrated as amount of evaporated water (mean +/- SD g/m2h) was less in the patients with PD than in the control participants on the dorsal parts of the hand (13.7 +/- 5.2 vs. 23.9 +/- 5.5, p < 0.001) and foot (16.0 +/- 6.0 vs. 22.1 +/- 8.3, p < 0.05). On the dorsal part of the hand, sweating in the patients with PD at Yahr stages I and II was less than that in the control-Participants (15.2 +/- 6.3 vs. 23.9 +/- 5.5, p < 0.05). Sweating in the patients with PD at Yahr stages III and IV was less than that in the control participants on the dorsal parts of the hand (10.8 +/- vs. 2.7 vs. 23.9 +/- 5.5, p < 0.001), and foot (10.9 +/- 2.3 vs. 22.1 +/- 8.3, p < 0.005). Sweating on the dorsal part of the foot was less in the patients with PD at Yahr stages III and IV than that in those at Yahr stages I and II (10.9 +/- 2.3 vs. 18.4 +/- 6.1, p < 0.05). Sweating on the forehead in the patients with PD at Yahr stages I and II stage was slightly but not significantly less than that in the control participants (21.8 +/- 3.8 vs. 32.7 +/- 11.9, p < 0.2). Sweating on the forehead in the patients with PD at Yahr stages III and IV was sightly but not significantly greater than that in those at Yahr stages I and II (25.4 +/- 5.6 vs. 21.8 +/- 3.8, p < 0.2). Increased sweating on the forehead skin might compensate for decreased sweating on the extremital skin. Our results suggest that sudomotor dysfunction in PD primarily affects the distal parts of the upper and lower extremities. Sudomotor dysfunction affecting distal parts of the extremities worsens with increased severity of PD.

Aged↗

Autonomic neural dysfunction in recently diagnosed diabetic subjects.

Because onset of autonomic neural dysfunction in the diabetic syndrome has not been well established, sensitive and quantitative measures of autonomic nervous system (ANS) function were made in 19 non-insulin-dependent (NIDD) and 14 insulin-dependent (IDD) recent-onset diabetic subjects. The known duration of diabetes mellitus in the NIDD subjects was less than or equal to 12 mo. The duration in the IDD subjects was less than or equal to 24 mo. RR-variation during beta adrenergic blockade (an index of an ANS reflex involving the cardiac parasympathetic nervous system [PNS] pathway) was smaller than that of control subjects in both NIDD (P less than 0.001) and IDD subjects (P less than 0.01). This PNS abnormality was not likely to be due to volume depletion since acute volume depletion induced by furosemide in six normal subjects (1608 +/- 105 ml, mean +/- SEM) did not change RR-variation. Dark-adapted pupil size after topical PNS blockade (an index of iris sympathetic nervous system [SNS] activity) was also smaller in both groups of diabetic subjects (NIDD, P less than 0.01; IDD, P less than 0.05). Pupillary latency time (an index of an ANS reflex involving iris PNS pathway) was prolonged in the NIDD subjects (P less than 0.005) but was not significantly altered in the IDD subjects. Thus, it would appear that the ANS is impaired soon after the diagnosis of diabetes mellitus. We hypothesize that early impairment of the ANS is common in IDD and NIDD subjects. This finding is consistent with the hypothesis that abnormal carbohydrate metabolism is an important factor in the etiology of diabetic autonomic neuropathy.

Adult↗

Biochemical changes in multiple system atrophy detected with positron emission tomography.

Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder manifested by parkinsonism and dysfunction of autonomic, cerebellar, urinary, and pyramidal systems. The most frequent presentation is with a combination of parkinsonism and autonomic dysfunction, but cerebellar ataxia with autonomic failure occurs frequently as well. Striatonigral degeneration (SND) and sporadic olivopontocerebellar atrophy (sOPCA) can progress to include autonomic failure and thus may be forms of MSA, but it is not known whether all such cases progress to MSA. Utilizing positron emission tomography (PET) with various ligands, my colleagues and I have investigated the biochemical changes in sOPCA and MSA to understand the relationship between these disorders. An initial study revealed decreased local cerebral metabolic rates for glucose in the brainstem, cerebellum, putamen, thalamus and cerebral cortex in both MSA and sOPCA, suggesting that many sOPCA patients would evolve to develop MSA. Later studies confirmed this by demonstrating decreased monoaminergic nigrostriatal terminals in both sOPCA and MSA patients. The studies suggest that the ligand used might be helpful in determining the risk that an individual patient with sOPCA will progress to develop MSA. An investigation of the course of sOPCA patients observed clinically over several years revealed that approximately one-fourth of them progress to MSA within five years. Studies of gamma-aminobutyric acid type A/benzodiazepine neurotransmitter receptors revealed that these sites are largely preserved in sOPCA and MSA, indicating that symptomatic pharmacological therapy may be possible in these disorders.

Journal Article↗

Effect of PUVA therapy on electrodermal activity parameters in vitiligo patients.

UNLABELLED: Recent electrophysiological studies on autonomic dysfunction in vitiligo patients show an autonomic dysfunction as measured by absent sympathetic skin response (SSR). Nothing is known about the reversibility of these autonomic parameters with treatment. The present study examined how Electrodermal Activity (EDA) parameters were affected from vitiligo illness before PUVA therapy and whether any electrophysiological gains acquired from PUVA therapy would influence the progression of the condition itself. We studied in 14 healthy subjectS and 14 patients with generalized vitiligo before and after treatment. EDA was recorded with a skin conductance unit connected to a personal computer. Before treatment, skin conductance level (SCL) and habituation number (HN) was higher in vitiligo group than control groups. After treatment, SCL and HN were decreased nearly to normal value. Before and after treatment, prevalence of non-responsivity was higher in vitiligo group than controls. CONCLUSION: The sympathetic nervous system might have a particular role in the pathogenesis of vitiligo. Thus, patients with vitiligo may have changes to EDA parameters that are reversible to great extent with PUVA therapy. EDA is a useful method of studying the autonomic dysfunction in humans.

Adolescent↗

Clinical investigation on hypotensive patients with vertigo.

The aim of this study was to investigate the characteristic of hypotensive patients with vertigo. Twenty hypotensive patients with rotatory vertigo, 15 hypotensive subjects without vertigo, and 15 mitral valve prolapse subjects without vertigo underwent a battery of tests including audiometry, electronystagmography (ENG), and vestibular evoked myogenic potential (VEMP) test. The abnormal rates in terms of audiometry, eye tracking, optokinetic nystagmus, visual suppression, and caloric tests were 15, 35, 35, 10, and 42% for the first group; 13, 20, 33, 0, and 0% for the second group; and 7, 13, 60, 0, and 3% for the third group, respectively. Comparison of the first group with the other two control groups revealed that significant difference existed only in the abnormality of caloric responses. Fifteen (75%) of 20 hypotensive patients with vertigo having abnormal ENG results, asymmetric caloric responses, or delayed VEMPs were attributed to vertigo of central origin, possibly from ischemic disorder. In contrast, five patients (25%) had neither central signs in ENG nor abnormal VEMPs, but showing bilateral normal or hyperactive caloric responses were classified as autonomic dysfunction. After 3 months of medication, all patients with autonomic dysfunction had their vertigo and autonomic symptoms subsided, whereas 27% of the patients with ischemic disorder had vertigo persisted, showing a significant difference. In conclusion, hypotensive patients with vertigo could be due to either direct autonomic dysfunction or ischemic disorder mediated by autonomic deficits.

Adult↗

[Abnormal sensation in the throat and autonomic nerve dysfunction symptoms].

Abnormal sensations, such as a lump, itchiness or choking, in the throat (AST) may develop as symptoms of autonomic nerve dysfunction (AND). If this is true, the subjects with AST should show more subjective symptoms and objective signs of AND than those without AST. We classified 500 otolaryngological and neurological patients [172 males and 328 females, age 58.4 +/- 14.0 years (mean +/- SD)] with various signs and symptoms suggesting autonomic nerve dysfunction into 2 groups: 370 patients with AST (AST group) and 130 without AST (non-AST group). For the subjective evaluation of AND symptoms, we calculated the number of positive answers to 33 questions concerning AND symptoms which appear in the Cornell Medical Index (Health Questionnaire). Objective evaluation of AND was done by analyzing the coefficient of variation (%) of 100 R-R intervals on electrocardiograms [CV R-R (%)], as previous studies by others have shown that CV R-R (%) decreases with age and/or with the severity of autonomic nerve dysfunction. The following results were obtained in the comparison between the two groups. 1) There were significantly more complaints of AND symptoms in the AST group (7.3 +/- 5.5, mean +/- SD) than in the non-AST group (5.3 +/- 4.4) (p < 0.0005 by Wilcoxon test). 2) The relative CV R-R (%) value calculated by dividing the CV R-R (%) actually obtained by the formula [5.13 - 0.0419 x age of subject (years)] was significantly smaller in the AST group (0.98 +/- 0.40) than in the non-AST group (1.06 +/- 0.39) (p < 0.05 by Wilcoxon test).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Peripheral autonomic nerve dysfunction in asymptomatic leprosy contacts.

In endemic areas, subclinical autonomic nerve dysfunction may be a manifestation of infection with M. leprae and possibly allow detection before progression to clinical disease. Vasomotor reflex (VMR) testing was performed in 36 asymptomatic leprosy contacts (24 household contacts, 12 hospital contacts) and 47 age- and sex-matched controls in Pokhara, Nepal. Mean age was 30 years, two thirds were male. A Moor instruments DRT4 laser doppler monitor was used for velocimetry of microvascular blood flow. The flow reduction following an inspiratory gasp was recorded from finger and toe tips. Mean percent reduction was 57.8 (standard deviation 14.6) among household contacts, 61.9 (17.5) among hospital contacts and 66.8 (7.8) among controls (p=0.001 by analysis of variance). The prevalence of abnormal test results was 54% among household contacts, 42% among hospital contacts and 15% among controls (p=0.0005 by chi-square test for trend). Subclinical autonomic neuropathy is common among healthy contacts of leprosy patients. Prospective studies are now needed to clarify to what extent abnormal VMR tests predict the risk of progression to clinical disease.

Adult↗

Asthma, asthma medication and autonomic nervous system dysfunction.

Asthma is associated with autonomic nervous imbalance: an increased bronchial sensitivity to cholinergic constrictors and possibly a decreased sensitivity to beta2-adrenergic dilators have been reported in this disease. Also, non-adrenergic and non-cholinergic (NANC) mediators have a small regulatory effect on airway function. These mediators contribute to the pathogenesis of asthma not only by regulating smooth muscle tone in the airways but also by affecting pulmonary blood flow, endothelial permeability and airway secretions. In many studies increased parasympathetic responsiveness has been associated with clinical asthma or the worsening of asthma in adults. However, most of the studies in children have not found association between autonomic dysfunction and asthma. Therefore, the autonomic dysfunction in asthma may be related to more advanced disease or long-term asthma medication in adults. This article briefly reviews the relationships between airway inflammation, beta2-agonist, anticholinergic and glucocorticoid medication as well as autonomic nervous function in asthma.

Adrenergic beta-Agonists↗