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At least 757 records · Page 42Linked to original sources
PubMed2002

Degenerative and inflammatory lesions in sympathetic ganglia: further morphological evidence for an autonomic neuropathy in AIDS.

There is accumulating evidence that autonomic dysfunction occurs in HIV infection. While many studies have demonstrated autonomic abnormalities on clinical basis, only one has studied the morphology of sympathetic ganglia. The superior sympathetic ganglia of 12 randomly selected AIDS patients and those of 6 controls were examined morphologically in order to determine the frequency and severity of their involvement. Although they had not been investigated for autonomic dysfunction, 5 had suffered from non-infectious diarrhoea, one showed bilateral ptosis and another had non-specified visual problems. All cases showed clusters, and perivascular mononuclear inflammatory cells, occasionally infiltrating vessel walls, some evidence of nerve cell degeneration, and proliferation of capsule cells. Immunostainings showed T lymphocytes and an increased number of macrophages. HIV antigens were detected in macrophages, in 6 cases (50%). This study provides further morphological support for the autonomic dysfunction in association with HIV infection. As for the mechanism of this dysfunction, it has been postulated a direct infection, the virus entering the ganglia through macrophages and acting as a reservoir for HIV, and an autoimmune pathogenesis. Since HIV antigens were not detected in 50% of the cases in this and in a previous study, despite the existence of morphological lesions, it is possible that, as in HIV-related sensory-motor peripheral neuropathies, an autoimmune mechanism may also play a role in the development of the autonomic lesions.

AIDS Dementia Complex↗
PubMed1991

Assessment of early stage autonomic nerve dysfunction in diabetic subjects--application of power spectral analysis of heart rate variability.

To assess early stage autonomic nerve dysfunction, power spectral analyses were conducted on the consecutive RR records of healthy subjects (N/C, n = 21) and age-matched diabetic patients without neuropathy (DNN, n = 11), with peripheral neuropathy alone (DPN, n = 14), and with autonomic neuropathy (DAN, n = 13) during resting, deep breathing, and tilting. From the analyses, power spectral densities of low frequency (0.05-0.1 Hz) component (LF; msec2) and of high frequency (0.2-0.35 Hz) component (HF; msec2) were calculated as expressing sympathetic activity and parasympathetic activity, respectively. In N/C, LF and HF were 466 +/- 332 and 251 +/- 151, respectively. Deep breathing significantly (p less than 0.05 by paired t-test) increased HF to 403 +/- 305 and tilting increased LF significantly to 593 +/- 375. In diabetics as a group, both LF and HF were significantly smaller than those in N/C. DNN showed significantly smaller HFs than N/C. DPN showed a significantly smaller HF during deep breathing (135 +/- 93) and a significant smaller LF during tilting (122 +/- 119) than N/C. DAN showed a significantly smaller HF during deep breathing (49 +/- 49) and a significantly smaller LF during tilting (54 +/- 52) than DPN. Tilting increased LF significantly (p less than 0.001) in N/C but not in diabetics. Deep breathing increased HF significantly (p less than 0.001) in N/C and DNN. HF in diabetics highly correlated with known duration of diabetes. LF in diabetics did not correlate with known duration of diabetes nor level of hemoglobin A1c.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Adventitial dysfunction: an evolutionary model for understanding atherosclerosis.

Endothelial and smooth muscle dysfunctions are widely implicated in the pathogenesis of atherosclerosis. Modern mechanical and pharmacologic treatments aim to remodel abnormalities of the vessel intima and media. We hypothesize that adventitial dysfunction comprises the dominant source of atherosclerosis by originating many endothelial and smooth muscle abnormalities. The autonomic nervous system innervates the adventitia, and autonomic dysfunction induces many end-organ dysfunctions including inflammation and thrombosis. The link between diabetes and atherosclerosis may operate through adventitial autonomic neuropathy. Smoking may promote atherosclerosis by inducing adventitial autonomic dysfunction related to nicotine-mediated compensatory upregulation of sympathetic bias independent of endothelial injury induced by purported tobacco toxins. While hypertension is thought to cause atherosclerosis, the two conditions may instead represent independent consequences of autonomic dysfunction. The link between aging and atherosclerosis may operate through adventitial dysfunction induced by autonomic dysregulations. Exercise may ameliorate atherosclerosis by restoring adventitial autonomic function, thereby normalizing adventitial regulation of medial and intimal biology. Feed-forward adventitial vascular baroreceptor and chemoreceptor dysregulation may further exacerbate atherosclerosis as intimal plaque interferes with these sensors. Since penetrating external physical injury likely represented a dominant selective force during evolution, the adventitia may be preferentially equipped with sensors and response systems for vessel trauma. The convergent response of adrenergia, inflammation, and coagulation, which is adaptive for physical trauma, may be maladaptive today when different stressors trigger the cascade. Endoluminal therapies including atherectomy, angioplasty, and stent deployment involve balloon expansion that traumatizes all layers of the vessel wall. These interventions may paradoxically reinitiate the cascade of atherogenesis that begins with adventitial dysfunction and leads to restenosis. Methods to reduce adventitial trauma, a maladaptive trigger of adventitial dysfunction, may reduce the risk of restenosis. We envision novel mechanical and biopharmaceutical solutions that target the adventitia to prevent or treat atherosclerosis including novel drug delivery strategies, exo-stents that wrap vessels, and neuromodulation of vessels.

Animals↗
PubMed1986

Use of alpha 2 adrenoreceptor agonists and antagonists in the functional assessment of the sympathetic nervous system.

We studied the effects of clonidine, an alpha 2-adrenoreceptor agonist, and yohimbine, an alpha 2-adrenoreceptor antagonist, on blood pressure, heart rate, and plasma catecholamines in 12 patients with autonomic dysfunction. Clonidine (0.1 mg, orally) lowered blood pressure 18 +/- 3 torr in six subjects and raised it 5 +/- 1 torr in six. The change in blood pressure in response to this dose of clonidine was inversely proportional to the supine level of norepinephrine (P less than 0.05). Yohimbine (4-64 micrograms/kg) raised plasma norepinephrine and blood pressure in six patients with degenerative autonomic dysfunction. Yohimbine also attenuated by 50% (P less than 0.05) the hypotensive response to head-up tilt of patients with degenerative autonomic dysfunction. Clonidine depends upon postjunctional hypersensitivity and the degree of autonomic insufficiency to elicit its pressor response. In contrast, the pressor response to yohimbine is related to the capacity of the sympathetic nervous system to be activated and release norepinephrine. If plasma norepinephrine levels following yohimbine administration are monitored, the biochemical and hemodynamic response to the drug may provide a sensitive indication of the capacity of the sympathetic nervous system to be activated in patients with autonomic dysfunction.

Adult↗
PubMed1983

[Function of the autonomic nervous system in children and adolescents with insulin-dependent diabetes mellitus].

19 IDDM patients (m/f 9/10; ages 7-25 y.; duration of diabetes 3-20 y., mean 10 y.) have been compared to 15 healthy controls (m/f 11/4; ages 11-24 y., mean 14 y.) in respect to HRTS (heart rate response to standing), SDB (single deep breath) and Valsalva maneuvre. In the diabetics the results have been correlated to MNCV (motor nerve conduction velocities), quality of diabetic control and duration of diabetes. A questionnaire did not uncover signs or symptoms of autonomic dysfunction. Resting heart rates were significantly higher in diabetics but were unrelated to age, duration of diabetes, quality of diabetic control or MNCV. HRTS, SDB and the Valsalva maneuvre did not display statistically significant differences between diabetics and controls. Diabetic autonomic dysfunction seems to be rare in young diabetics. Routinely testing for this sequela would therefore not be justified at this stage of diabetes. On the other hand diabetic autonomic dysfunction might be harmful for the patient as regards sudden and unexpected cardiorespiratory arrest eg. during anaesthesia or bronchopneumonia. If therefore symptoms and/or signs of possible peripheral or autonomic dysfunction are present special investigations (eg. HRTS) are indicated.

Adolescent↗
PubMed1998

Autonomic function and autoantibodies to autonomic nervous structures, glutamic acid decarboxylase and islet tyrosine phosphatase in adolescent patients with IDDM.

Recent studies have linked autoimmunity to nervous tissue structures and diabetic autonomic neuropathy, but data on the early stage of IDDM and on the natural history of this association are not available. For this reason, we investigated autonomic nervous function, and the presence of autoantibodies to sympathetic and parasympathetic nervous structures, to glutamic acid decarboxylase (GAD) and tyrosine phosphatase (IA-2/ICA512) in 85 adolescents with insulin-dependent diabetes mellitus (IDDM) (mean age 14.7+/-1.6 yr, mean duration of diabetes 6.8+/-3.5 yr), and 45 age and sex-matched healthy subjects. Nervous tissues autoantibodies were detected using an indirect immunofluorescent complement-fixation technique, with monkey adrenal gland, rabbit cervical ganglia and vagus nerve as substrates. GAD and IA-2/ICA512 autoantibodies were detected by radioimmunoprecipitation assay. Seven patients (8%) had anti-vagus nerve autoantibodies, 7 other patients (8%) had anti-cervical ganglia autoantibodies, while all controls were negative (P < 0.05). Anti-adrenal medulla antibodies were detected in 16 patients (19%) and in 2 control subjects (P<0.02). None of the patients had autonomic symptoms. When patients were divided according to the presence or absence of autoantibodies, values of the cardiovascular tests (deep breathing, 30:15 ratio, Valsalva ratio) were similar in the two groups and similar to those in healthy subjects. However, when considered together, patients positive for one or more autoantibody showed a trend for lower values of deep breathing test and 30:15 ratio test, compared with healthy control subjects, which failed to reach conventional significance values (P=0.17 and P=0.07, respectively). No correlation was found between cardiovascular parameters and metabolic control or diabetes duration. There was no association between autoimmunity to nervous tissue structures and presence of GAD and IA-2/ICA512 Ab, and no correlation between these two autoantibodies and values of cardiovascular tests. Our data indicate that autonomic dysfunction is not a characteristic of young diabetic patients, but that autoantibodies against autonomic nervous structures are present during the first 1 to 15 yr of diabetes. GAD and tyrosine phosphatase appear to be excluded as target autoantigens within autonomic structures. Follow-up studies are required to evaluate future autonomic dysfunction and symptoms in these patients, and to establish whether the subtle autonomic dysfunction detected and/or the nervous tissue autoantibodies, are predictive of the development of this complication.

Adolescent↗
PubMed1985

Estimation of plasma and urinary catecholamines in Guillain-Barré syndrome.

Serial estimation of plasma nor-epinephrine (PNE), 24 hours urinary vanilmandelic acid (VMA) and plasma cortisol was made in 25 adult patients of Guillain-Barré syndrome. Healthy adult age and sex matched volunteers served as controls. The mean level of PNE, VMA and plasma cortisol in controls was 1.07 +/- 0.50 ng/ml, 2.81 +/- 1.18 mg/24 hours and 12.9 +/- 3.10 micrograms/100 ml, respectively. In cases of Guillain-Barré syndrome with autonomic dysfunction the mean level of PNE, VMA and plasma cortisol was 3.34 +/- 2.47 ng/ml, 7.98 +/- 5.71 mg/24 hours and 27.25 +/- 4.94 micrograms/100 ml on the day of admission while in cases of Guillain-Barré syndrome without autonomic dysfunction it was 1.09 +/- 0.32 ng/ml, 3.04 +/- 2.22 mg/24 hours and 11.8 +/- 4.2 micrograms/100 ml, respectively. An increase in circulating PNE, VMA and plasma cortisol was demonstrated in patients of Guillain-Barré syndrome with autonomic dysfunction presenting as hypertension and tachycardia. The maximum rise of 284% (PNE) and 253% (VMA) occurred at the height of paralysis. The elevated levels fell to near control values at the time of significant recovery, and glucose tolerance tests improved. It is suggested that increased levels of catecholamines and cortisol contributed to the development of dysautonomia as these levels were within normal limits in patients of Guillain-Barré syndrome without autonomic dysfunction.

Adolescent↗
PubMed2001

Substance P immunoreactivity in the enteric nervous system in Rett syndrome.

Rett syndrome is associated with profound mental retardation and motor disability in girls. It has a characteristic clinical phenotype which includes abnormalities of the autonomic nervous system. Feeding impairment and severe constipation are two symptoms of this autonomic dysfunction. Substance P, an important peptide in the autonomic nervous system, is decreased in the cerebrospinal fluid of Rett syndrome. We have demonstrated that substance P immunoreactivity is significantly decreased in Rett syndrome brain-stem and may be related to the autonomic dysfunction. In this study, we have continued the investigation of substance P in the enteric nervous system. We immunohistochemically examined the normal developing bowel in 22 controls (ages, 14 gestational weeks to 31 years) using formalin fixed tissue, with antibodies to substance P, tyrosine hydroxylase and vasoactive intestinal peptide. We compared the immunoreactivity of normal controls with 14 cases of Rett syndrome (ages, 5-41 years) and observed that the expression of substance P, tyrosine hydroxylase and vasoactive intestinal peptide immunoreactivity in the bowel in Rett syndrome was not significantly different from that of controls. This suggests that the feeding impairment and constipation in Rett syndrome relate to dysfunction of the autonomic nervous system originating outside of the bowel, in the brain-stem, as suggested by our previous study.

Adolescent↗
PubMed2002

Clonidine-induced hypertension in a patient with a spinal lesion.

OBJECTIVE: To report a case of possible clonidine-induced hypertension (by Naranjo score) in a patient with a C4 spinal lesion. BACKGROUND: Clonidine is a medication long used to treat hypertension, and it is still used in the treatment of refractory hypertension. Although effective, clonidine use is hindered by adverse effects and its dual mechanism of action. CASE SUMMARY: A 39-year-old white, quadriplegic man with poorly controlled pain displayed many characteristics consistent with autonomic dysfunction (e.g., C4 spinal lesion, orthostatic hypotension, hypertension). The patient was routinely receiving transdermal clonidine and also received transdermal nitroglycerin paste as needed for control of acute hypertensive episodes. On the recommendation of the home healthcare pharmacists, clonidine was discontinued. Since that time, the patient's blood pressure and the use of emergent antihypertensive treatment have decreased significantly (maximum systolic and diastolic BP by approximately 50 and 25 mm Hg, respectively). CONCLUSIONS: Many of the characteristics of autonomic dysfunction, such as refractory hypertension, can seem selective for the use of clonidine and, because of its reliance on central alpha(2)-activity for its hypotensive effects, clonidine may induce hypertension in patients with autonomic dysfunction. Clonidine should be used with great caution when autonomic dysfunction is suspected.

Adrenergic alpha-Agonists↗
PubMed1995

Memory dysfunction and autonomic neuropathy in non-insulin-dependent (type 2) diabetic patients.

Considering the nervous system as a unit, it might be expected that diabetic patients with autonomic neuropathy could have a central abnormality expressed as cognitive dysfunction. To determine whether autonomic neuropathy is independently associated with cognitive dysfunction, we studied a cross-section of 20 non-insulin-dependent diabetic patients with autonomic neuropathy (14 males and six females; age (mean) = 60 + or - 1 years); 29 non-insulin-dependent diabetic patients without autonomic neuropathy (14 males and 15 females; age = 59 + or - 1 years) and 34 non-diabetic patients (10 males and 24 females; age = 58 + or - 1 years), matched by age, education and duration of disease. Cognitive function was evaluated by tests of immediate, recent and remote memory: verbal (digit span; word span) and visual (recognition of towers and famous faces). Diabetic patients with autonomic neuropathy scored (median) lower in visual memory tests than diabetic patients without autonomic neuropathy and controls (towers immediate = 5 versus 7 and 6; towers recent = 4 versus 6 and 6; faces = 16 versus 18 and 18; respectively; Kruskal-Wallis; P < 0.05). There was no difference in verbal memory performance (Kruskal-Wallis; P > 0.05). Entering age, education, duration of disease and fasting plasma glucose in a stepwise multiple regression, the performance in these tests remained associated with autonomic neuropathy (towers immediate, P = 0.0054, partial r2 = 0.166; towers recent, P = 0.0076, partial r2 = 0.163). Scores in visual tests correlated negatively with the number of abnormal cardiovascular tests (faces, r = -0.25; towers recent, r = -0.24; Spearman; P < 0.05). Decreased visual cognitive function in non-insulin-dependent diabetic patients is associated with the presence and degree of autonomic neuropathy.

Adult↗
PubMed2004

Cardiac autonomic neuropathy in the diabetic patient: does 123I-MIBG imaging have a role to play in early diagnosis?

OBJECTIVES: In diabetes, extended adrenergic receptor stimulation with hyperglycemia and insulin deficiency is associated with cardiac autonomic dysfunction. Clinically evident diabetic cardiac autonomic neuropathy (CAN) is associated with a poor prognosis. Research studies indicate that autonomic function tests, which are traditionally used to diagnose diabetic CAN, are less sensitive than (123)I-metaiodobenzylguanidine (MIBG) imaging, particularly in the early stages of the disease. This established imaging technique makes use of the noradrenaline analog MIBG, which is radiolabeled with (123)I to assess the noradrenaline uptake-1 mechanism of the sympathetic nervous system. Although scintigraphic studies indicate that long-standing cardiac autonomic dysfunction is permanent, some authors have shown partial reversibility with early metabolic intervention. (123)I-MIBG imaging could therefore have an important clinical role to play in the early diagnosis and treatment monitoring of diabetic CAN. METHODS: A PubMed/MEDLINE Internet search was performed using MIBG, diabetes, and cardiac autonomic neuropathy as key words. CONCLUSION: The general expense of (123)I-MIBG imaging, together with the lack of commercial availability of this radiopharmaceutical in the United States, has limited the clinical use of this technique. As such, the clinical role of (123)I-MIBG imaging in the early diagnosis of diabetic CAN has yet to be validated and defined in most regions of the world, and further study is required.

3-Iodobenzylguanidine↗
PubMedDate not supplied

[Autonomic cardiovascular dysfunction in multiple sclerosis not caused solely by brain stem lesions].

INTRODUCTION: Multiple sclerosis (MS) can cause alterations in autonomic cardiovascular functioning. Some authors attribute these anomalies detected in MS patients to brain stem lesions, due to the fact that important autonomic nuclei are located in this region of the brain. Other studies, however, have been unable to prove such a relation. AIMS. The purpose of this study was to analyse whether these alterations had an exclusive relation with the brain stem lesions that usually appear in the course of this disease. PATIENTS AND METHODS: We compared the spectral analysis of the heart rate variability (SAHRV) in the frequency domain between a group of 34 patients with MS and another group of 14 patients with isolated brain stem lesions (IBSL) of a non inflammatory origin, which were measured using a 24 hour Holter recording. RESULTS: Heart rate, very low rates, low rates and the low rate/high rate quotient are significantly higher in the MS group than in the IBSL group, even when the former present brain stem lesions. Results in the high rate component, however, depend on the presence of brain stem lesions in the MS group. CONCLUSION: These findings suggest that autonomic cardiovascular dysfunction in MS is only related with brain stem lesions, although we obtained results that confirm the importance of this area in cardiovascular innervation.

Adult↗
PubMed2006

Circadian rhythm of the autonomic nervous system in insulin resistant subjects with normoglycemia, impaired fasting glycemia, impaired glucose tolerance, type 2 diabetes mellitus.

BACKGROUND: In type 2 diabetes mellitus both insulin resistance and hyperglycemia are considered responsible for autonomic dysfunction. The relation between the autonomic activity, impaired fasting glycemia and impaired glucose tolerance is, however, unclear. The purpose of this study was to evaluate and compare the circadian autonomic activity expressed as heart rate variability (HRV) measured by 24-hours ECG recording in insulin resistant subjects (IR) with characteristics as follow: IR subjects with normal oral glucose tolerance test results, IR subjects with impaired fasting glucose, IR subjects with impaired glucose tolerance and subjects with type 2 diabetes mellitus. METHODS: Eighty Caucasian insulin resistant subjects (IR) and twenty five control subjects were recruited for the study. IR subjects were divided into four groups according to the outcoming results of oral glucose tests (OGTTs): IR subjects with normal glucose regulation (NGR), IR subjects with impaired fasting glycemia (IFG), IR subjects with impaired glucose tolerance (IGT) and subjects with type 2 diabetes mellitus (DM). Autonomic nervous activity was studied by 24-hours ECG recording. Heart rate variability analysis was performed in time and frequency domains: SDNN, RMS-SD, low frequency (LF) and high frequency (HF) were calculated. RESULTS: The total SDNN showed statistically significant reduction in all four groups with insulin resistant subjects (IR) when compared to the control group (p <0,001). During night LF normalized units (n.u.) were found to be higher in all four groups including IR subjects than in the control group (all p < 0,001) and subjects with normal glucose regulation (NGR), with impaired fasting glycemia (IFG) and with impaired glucose tolerance (IGT) were found to have higher LF n.u. than those in the type 2 diabetes mellitus group. The linear regression model demonstrated direct association between LF values and the homeostasis model assessment-index (HOMA-I), in the insulin resistant group (r = 0,715, p <0,0001). CONCLUSION: The results of our study suggest that insulin resistance might cause global autonomic dysfunction which increases along with worsening glucose metabolic impairment. The analysis of sympathetic and parasympathetic components and the sympathovagal balance demonstrated an association between insulin resistance and sympathetic over-activity, especially during night. The results indicated that the sympathetic over-activity is directly correlated to the grade of insulin resistance calculated according to the HOMA-I. Since increased sympathetic activity is related to major cardiovascular accidents, early diagnosis of all insulin resistant patients should be contemplated.

Adult↗
PubMed2004

Vasomotor rhinitis update.

PURPOSE OF REVIEW: This review was conducted to examine new data on vasomotor rhinitis, a common clinical problem. RECENT FINDINGS: Recent publications highlight advances in the study of the pathophysiology of vasomotor rhinitis. Electron microscopic and ultracytochemical evaluation of the nasal mucosa in vasomotor rhinitis demonstrates an emerging role of neuropeptides and nitric oxide in the pathogenesis of vasomotor rhinitis. Ozone, cigarette smoke, and other environmental factors may trigger neurogenic mechanisms that lead to vasomotor rhinitis. Objective tests have documented the presence of hypoactive sympathetic autonomic dysfunction. Such assessments also suggest autonomic dysfunction as a possible link between vasomotor rhinitis and gastroesophageal reflux disease. Recent publications propose nasal secretory protein analysis as a possible diagnostic tool. Evidence-based review of treatment outcomes shows topical sprays of azelastine, budesonide, and ipratropium to be of benefit in vasomotor rhinitis. SUMMARY: A better understanding of the role of nitric oxide and neuropeptides in the pathogenesis of vasomotor rhinitis has opened new avenues in research, diagnosis, and management. Clinical diagnosis may be aided by the analysis of nasal secretory proteins. Effective treatments include antihistamine, anticholinergics, and steroid nasal sprays.

Autonomic Nervous System↗
PubMed2004

Vascular dysfunction and autonomic neuropathy in Type 2 diabetes.

AIMS: To test the hypothesis that arterial dysfunction in Type 2 diabetes is related to autonomic neuropathy. METHODS: Arterial function and autonomic neuropathy were assessed over two consecutive days in 45 Type 2 diabetic and control subjects. Systemic arterial compliance (SAC), arterial stiffness (pulse-wave velocity, PWV) and carotid intima thickness (IMT) were assessed; these markers reflect early vascular disease and predict clinical vascular events. Autonomic neuropathy was assessed using heart rate variability with continuous ECG recording during various breathing and postural manoeuvres and an overall autonomic score was generated. Fasting metabolic parameters including glucose, insulin, HbA(1c) and lipid profile were measured. RESULTS: Autonomic neuropathy tests were all repeatable in diabetic subjects. Compared with controls, diabetic subjects had arterial dysfunction with increased PWV (P = 0.009), IMT (P < 0.001) and reduced SAC (P = 0.053). After adjustment for age, central PWV correlated with fasting insulin (r(2) = 0.45, P < 0.05) and autonomic score (r(2) = 0.44, P < 0.05), peripheral PWV correlated with autonomic score (r(2) = 0.51, P < 0.005) and IMT correlated with fasting insulin (r(2) = 0.5, P < 0.005). The presence of autonomic neuropathy correlated with fasting insulin (P = 0.015), but not age, duration diabetes, lipids or blood pressure. CONCLUSION: Using repeatable measures of autonomic neuropathy and vascular function in Type 2 diabetic subjects, we have demonstrated associations between autonomic neuropathy, vascular dysfunction and hyperinsulinaemia. This may help to explain the excess cardiovascular mortality seen in diabetic subjects with autonomic neuropathy.

Aged↗
PubMed2000

The use of clonidine in the management of autonomic overactivity in neuroleptic malignant syndrome.

The aim of this study was to identify the effectiveness of clonidine in the recovery of patients with neuroleptic malignant syndrome and autonomic dysfunction, including blood pressure lability. Nine patients with neuroleptic malignant syndrome and autonomic dysfunction were treated with clonidine in the intensive care unit, according to a protocol, and the results were compared with those of seven patients with the same syndrome who were not treated with clonidine. Clonidine was administered until blood pressure stability was fully restored, and thereafter the dose was gradually reduced. There was a significant reduction in the duration of ventilation and stay in the intensive care unit in the clonidine group. Three patients from the nonclonidine group died. The data suggest that in the clonidine group, patients with neuroleptic malignant syndrome and autonomic dysfunction appear to have better and faster recovery, especially in blood pressure control, after intravenous clonidine treatment.

Adrenergic alpha-Agonists↗
PubMed2005

Autonomic neural functions in space.

Autonomic neural functions are important to regulate vital functions in the living body. There are different methods to evaluate indirectly and directly autonomic, sympathetic and parasympathetic, neural functions of human body. Among various methods, microneurography is a technique to evaluate directly sympathetic neural functions in humans. Using this technique sympathetic neural traffic leading to skeletal muscles (muscle sympathetic nerve activity; MSNA) can be recorded from human peripheral nerves in situ. MSNA plays essentially important roles to maintain blood pressure homeostasis against gravity. Orthostatic intolerance is an important problem as an autonomic dysfunction encountered after exposure of human beings to microgravity. There exist at least two different types of sympathetic neural responses, low and high responders to orthostatic stress in orthostatic hypotension seen in neurological disorders. To answer the question if post-spaceflight orthostatic intolerance is induced by low or high MSNA responses to orthostatic stress, MSNA was microneurographically recorded for the first time before, during and after spaceflight in 1998 under Neurolab international research project. The same activity has been recorded during and/or after ground-based short- and long-term simulations of microgravity. MSNA was rather enhanced on the 12(th) and 13(th) day of spaceflight and just after landing day. Postflight MSNA response to head-up tilt was well preserved in astronauts who were orthostatically well tolerant. MSNA was suppressed during short-term simulation of microgravity less than 2 hours but was enhanced after long-term simulation of microgravity more than 3 days. Orthostatic intolerance after exposure to long-term simulation of microgravity was associated with reduced MSNA response to orthostatic stress with impaired baroreflex functions. These findings obtained from MSNA recordings in subjects exposed to space as well as short- and long-term simulations of microgravity indicate that sympathetic neural control is lowered when exposed to short-term microgravity but becomes enhanced after exposure to long-term microgravity. A lack of enhanced sympathetic neural response to orthostatic stress may induce orthostatic intolerance. Based on these findings effective countermeasures should be developed to prevent autonomic dysfunctions induced by exposure to microgravity. These include development of prescription and devices of physical exercise, electrical and magnetic nerve stimulations, body vibration, elastic bandage and stocking, lower body negative pressure, artificial gravity, medical drugs, and combinations of them. These countermeasures will be beneficial to prevent autonomic dysfunctions related to gravitational stress such encountered in bedridden subjects as orthostatic hypotension, atrophy of antigravity muscles and so on. This is particularly important in the present aged-society with many bedridden elderly people. The knowledge accumulated from studies on autonomic neural functions in space should be very useful to establish effective countermeasures and preventive methods for gravity-dependent autonomic dysfunctions.

Aging↗