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PubMed1989

VIP and autonomic neurotransmission.

A variety of peptides have been proposed as transmitter candidates in non-cholinergic, non-adrenergic nerves. The nerves containing vasoactive intestinal polypeptide (VIP), which innervate blood vessels, non-vascular smooth muscle, mucosal epithelium and glands comprise a major and wide-spread population of the peptide-containing systems. There is now experimental data supporting the view that VIP is a transmitter in non-adrenergic, non-cholinergic nerves in the digestive tract, respiratory tract and urogenital tract, controlling smooth muscle tone and motility, blood flow and secretion. It is possible that impairment of VIP-containing nerves is involved in a number of autonomic dysfunctions.

Animals↗

PubMed2005

Visual hallucinations in the diagnosis of idiopathic Parkinson's disease: a retrospective autopsy study.

BACKGROUND: For many years, visual hallucinations (VH) in idiopathic Parkinson's disease (PD) were thought to be a complication of antiparkinsonian treatment. The cause of VH is now thought to be nerve-cell loss and Lewy-body pathology in the ventral-temporal regions of the brain. However, the use of VH as a clinical sign of PD has not been investigated. METHODS: 788 cases with parkinsonism archived at the Queen Square Brain Bank for Neurological Diseases were identified for study. Patients had not been given standardised antemortem assessments. Clinical records were assessed for reports of VH. The incidence of VH in pathologically diagnosed cases was calculated, and factors affecting onset of VH were investigated. FINDINGS: VH occurred in 50% (221/445) of patients with PD, in 73% (32/44) with dementia with Lewy bodies (DLB), and in only 7% (18/255) of patients with non-Lewy-body parkinsonism. The specificity of VH for Lewy-body parkinsonism (PD and DLB combined) was 92.9% (95% CI 89.1-95.8) and the positive predictive value was 93.4% (89.7-95.8). VH were associated with cognitive dysfunction (hazard ratio 5.62, 3.37-9.35), autonomic dysfunction (3.13, 1.77-5.52), axial rigidity (2.22, 1.26-3.85) within the first 2 years of disease onset and also age of onset (1.05, 1.03-1.07). In PD, the onset of VH typically occurred in the second half of the disease course, and time to onset of VH was only weakly correlated with use of selegiline (Spearman's rho 0.22, p=0.005) and ergot dopamine agonists (0.24, p=0.006) but not correlated with use of levodopa, amantadine, or anticholinergic drugs. INTERPRETATION: The presence of VH is helpful in the differentiation of PD from other non-Lewy-body causes of parkinsonism. We propose that VH be added, as a supportive criterion, to the operational clinical criteria for the diagnosis of PD.

Adult↗

PubMed1993

Physiological, symptomatic and hormonal responses to acute hypoglycaemia in type 1 diabetic patients with autonomic neuropathy.

The effects of peripheral autonomic neuropathy on the symptomatic, physiological, and hormonal responses to acute insulin-induced hypoglycaemia were studied in two groups of patients with Type 1 diabetes, matched for age, duration of diabetes, and prevailing glycaemic control. A group of eight patients who gave a history of normal awareness of hypoglycaemia and had normal cardiovascular autonomic function tests were compared to a group of six patients who had symptoms of autonomic dysfunction and gross abnormalities of cardiovascular autonomic function tests. An additional two patients with autonomic neuropathy who also had hypoglycaemia unawareness were studied. Acute hypoglycaemia was induced by intravenous infusion of insulin (2.5 mU kg-1 min-1) and the onset of the acute autonomic reaction (R) was identified objectively by the sudden rise in heart rate and onset of sweating. Cognitive function and hypoglycaemia symptom scores were estimated serially, and plasma counterregulatory hormones were measured. Acute autonomic activation was observed to occur in all subjects in response to hypoglycaemia and commenced at similar venous plasma glucose concentrations in both groups (neuropathic patients: 1.6 +/- 0.2 mmol l-1 vs non-neuropathic patients 1.6 +/- 0.2 mmol l-1, p = 0.9,). In the neuropathic patients plasma adrenaline responses were significantly lower at all time points from time R until time R + 30 min (MANOVA for repeated measures, F = 19.4, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

The middle cerebral artery flow velocities during head-up tilt testing in diabetic patients with autonomic nervous system dysfunction.

BACKGROUND: The goal of this study was to examine the effects of diabetes mellitus on the trend of mean arterial velocity (v(m)) in both middle cerebral arteries during head-up tilt (HUT). METHODS: The study was performed in 20 patients, 9 females and 11 males (mean age 51 +/- 12 years) with an average 17-year history of insulin-dependent diabetes mellitus type I or II and a dysfunction of the autonomic nervous system confirmed by cardiocirculatory tests [Valsalva maneuver, deep breathing test, handgrip test, orthostatic test and spectral analysis of heart rate (HR) variability], and 19 age-matched healthy volunteers, 9 females and 10 males (mean age 48 +/- 6.8 years). v(m) was measured by a transcranial Doppler monitoring system during a 5-min baseline period, followed by a 5-min HUT in the upright position (90 degrees ). Mean arterial blood pressure (MAP), HR and end-tidal CO(2) (Et-CO(2)) were monitored concomitantly. RESULTS: In healthy volunteers, v(m) decreased stepwise during the first minute of HUT, reaching a minimum during the last 2 min of the test (v(m): basal 63.0 +/- 11.7 cm/s, 1st min 57.6 +/- 12.2 cm/s, 2nd min 55.9 +/- 12.6 cm/s, 3rd min 53.4 +/- 12.6 cm/s, 4th min 52.1 +/- 12.7 cm/s, 5th min 51.3 +/- 13.5 cm/s). In the supine position, v(m) recovered and reached the resting v(m) values. It declined gradually during HUT and less steeply in diabetic (v(m): basal 54.4 +/- 10.1 cm/s, 1st min 51.96 +/- 9.3 cm/s, 2nd min 50.7 +/- 11.6 cm/s, 3rd min 50.5 +/- 11.4 cm/s, 4th min 49.5 +/- 10.7 cm/s, 5th min 48.8 +/- 11.5 cm/s) than in healthy subjects. v(m) differed significantly (p = 0.00) between rest and HUT in both groups. The differences in MAP, HR and Et-CO(2) during rest and HUT between the groups were not statistically significant (p DeltaMAP = 0.36, p DeltaHR = 0.86, p DeltaEt-CO(2) = 0.97). The results of the analysis of variance of v(m) for repeated measurements between the two groups of subjects were highly significant (p = 0.00). The model of linear regression analysis was significant (p = 0.007). Diabetes was significant in the model (p = 0.00), while DeltaMAP, DeltaHR and DeltaEt-CO(2) were not. CONCLUSIONS: These findings may indicate that vasomotor responses during HUT testing are decreased in diabetic patients.

Adult↗

PubMed1981

Reversible autonomic neuropathy and hypertrophic osteoarthropathy in a patient with bronchogenic carcinoma.

We report a case of adenocarcinoma of the lung with pandysautonomia and pulmonary osteoarthropathy. Surgical resection of the tumor followed by radiation therapy for the residual tumor resulted in complete resolution of arthropathy and almost complete recovery from autonomic dysfunction. The symptoms of arthropathy and autonomic neuropathy recurred simultaneously several months later with increase in the tumor mass as confirmed at second surgical exploration. The second thoracotomy revealed an inoperable tumor. Following the second thoracotomy, while the arthropathy was relieved, the autonomic neuropathy persisted. We concluded that autonomic neuropathy is related to the tumor mass, and pulmonary osteoarthropathy and autonomic neuropathy are probably caused by different mechanisms, as yet undefined.

Autonomic Nervous System Diseases↗

PubMed1994

Central autonomic dysorganization in the early stages of experimental meningitis in rabbits induced by complement-C5A-fragment: a pathophysiological validation of the largest lyapunov exponent of heart rate dynamics.

In a study of central autonomic organization in early stages of experimental meningitis in rabbits, the temporal oscillations of the momentary heart rate (heart rate dynamics) were measured. In 10 anesthetized rabbits an experimental meningitis was induced by intracisternal injection of complement-C5a-fragment in a carrier solution of sodium chloride and bovine serum albumin. 10 rabbits were injected with the above carrier solution only and served as controls. The temporal structure of the heart rate dynamics was operationalized phase-space analytically through the estimation of the largest Lyapunov exponent. Without exception, positive Lyapunov exponents of the heart rate dynamics were found, which revealed chaotic oscillations. In contrast to the controls, the intracisternal injection of C5a caused a significant decrease of the analytical index and reduced its reproducibility significantly. This result suggests a subtle central-autonomic dysfunction and a loss of the autonomic steady-state induced by the acute inflammatory process.

Animals↗

PubMed1995

[A case of subacute sensory neuropathy associated with extraovarian serous papillary adenocarcinoma of the peritoneum].

We reported a case of subacute sensory neuropathy. A 78-year-old woman was admitted to Kenwakai Hospital because of progressive numbness in her hands and feet. Four months before admission, numbness and tingling sensations appeared in her hands and feet, and subsequently she felt difficulty in skilled finger movement. On general examination, she was found to have a mass in the right lower abdomen. Neurological examination revealed marked loss of position sense and vibratory sense in the distal extremities, and mild reduction of sensation to pinprick and light touch in the distal extremities. Stretch reflexs were depressed in the upper limbs and absent in the lower limbs. Her gait was unsteady and Romberg's sign was positive. She showed no cranial nerve dysfunction, cerebellar ataxia, muscle weakness, and autonomic dysfunction. Blood examination revealed high TTT (11.3Kunkel U), high ZTT (16.4Kunkel U) titer. Tumor markers were normal except for CA125 (93 U/ml). The cerebrospinal fluid showed 48 mg/dl of protein, 10.6 mg/dl of IgG. and an almost normal cell count (5.3/mm3). Serum was tested by immunohistochemical staining. Only the cytoplasm of neurons in the dentate nucleus and brain stem was stained on a rat's brain. Sural nerve biopsy showed a severe loss of large myelinated fibers. An exploratory laparotomy revealed a peritoneal tumor, 5 cm in diameter, and it was removed. During the surgery, other than a few rice-sized nodules in the cul-de-sac, there was no evidence of tumor in bilateral ovaries. The tumor was proven to be a serous papillary adenocarcinoma with psammoma bodies resembling ovarian cancer.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1991

Aggregation of subclinical autonomic nervous system dysfunction and autoantibodies in families with type I diabetes.

The purpose of our study was to evaluate the occurrence of autonomic nervous system autoantibodies (ANS) in the nondiabetic family members of insulin-dependent (type I) diabetic subjects. We studied 24 families, including 45 nondiabetic parents and 53 nondiabetic siblings of a type I diabetic proband. One hundred one nondiabetic population control subjects were also studied. Stored sera from nondiabetic family members and control subjects were evaluated for the presence of complement-fixing (CF) adrenal medullary antibodies (CF-ADM), sympathetic ganglia antibodies (CF-SG), and vagus nerve antibodies (CF-V) by indirect immunofluorescence. HLA-DR3 and -DR4 typing was performed on 42 nondiabetic family members and 104 diabetic subjects. One or more CF-ANS were in 45 of 93 (40%) nondiabetic family members compared to 2 of 70 (2.8%) control subjects. CF-SG were in 28 of 92 (30%) family members compared to 0 of 101 control subjects (P = 0.0001). CF-V were in 25 of 95 (26%) family members compared to 0 of 76 control subjects (P = 0.0001). CF-ADM were in 10 of 83 (12%) family members compared to 2 of 70 (2.8%) control subjects (P = 0.056). There was no HLA-DR3 or HLA-DR4 association with ANS. Subclinical autonomic dysfunction was demonstrated in 3 of 4 family members with autoantibodies compared to 0 of 4 family members without autoantibodies.

Adolescent↗

PubMed2006

Quantitative studies of autonomic function.

Dysfunction of the peripheral and central autonomic nervous system is common in many neurological and general medical diseases. The quantitative assessment of sympathetic and parasympathetic function is essential to confirm the diagnosis of autonomic failure, to provide the basis for follow-up examinations, and potentially to monitor successful treatment. Various procedures have been described as useful tools to quantify autonomic dysfunction. The most important tests evaluate cardiovascular and sudomotor autonomic function. In this review, we therefore focus on standard tests of cardiovascular and sudomotor function such as heart-rate variability at rest and during deep breathing, active standing, and the Valsalva maneuver, and on the sympathetic skin response. These tests are widely used for routine clinical evaluation in patients with peripheral neuropathies. Refined methods of studying heart-rate variability, baroreflex testing, and detailed measures of sweat output are mostly used for research purposes. In this context, we describe the spectral analysis of slow modulation of heart rate or blood pressure, reflecting sympathetic and parasympathetic influences, and consider various approaches to baroreflex testing, the thermoregulatory sweat test, and the quantitative sudomotor axon reflex test. Finally, we discuss microneurography as a technique of direct recording of muscle sympathetic nerve activity.

Autonomic Nervous System↗

PubMed2004

Peroxisome proliferator ameliorates endocardial endothelial and muscarinic dysfunction in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) develop hypertension (HT) at the age of 2-6 weeks. Endocardial endothelial (EE) dysfunction, autonomic suppression, left ventricle hypertrophy (LVH), and fibrosis are hallmarks of HT. The mechanism of EE dysfunction, LVH, and fibrosis in SHR is largely unknown. It is known, however, that the levels of peroxisome proliferator-activated receptor gamma (PPARgamma) are negatively correlated with EE function, LVH, and HT. PPARgamma ameliorates EE dysfunction and LVH, in part, by increasing endothelial nitric oxide (eNO) and muscarinic activity. Male SHR and normotensive Wistar rats (NWR) at 1 week of age were administered 8 micro g/ml ciglitazone (CZ), a PPARgamma agonist, in drinking water. The rats were grouped as follows: NWR, NWR+CZ, SHR, SHR+CZ, at 2 and 6 weeks (n = 6 in each group). The levels of PPARgamma were low in the nuclear extracts of the left ventricle (LV) in SHR, but increased in CZ-treated rats, measured by western analysis. The contractile response to norepinephrine in cardiac rings prepared from the above groups of rats, measured in tissue myobath and normalized by tissue weight, demonstrated no difference in the maximum response to norepinephrine in any group. However, the EC(50) was significantly lower in SHR at 2 weeks (SHR2wk) than in any other groups, and CZ normalized this decrease. The response to acetylcholine demonstrated no difference in EC(50); however, the maximum response was attenuated in SHR2wk, and substantially increased in SHR6wk as compared with age-matched NWR, suggesting that early in HT eNO dysfunction in SHR2wk leads to depression of autonomic muscarinic cholinergic receptor in SHR6wk. The PPARgamma agonist ameliorated both the early eNO dysfunction and late autonomic suppression in HT. The response to nitroprusside demonstrated no change in EC(50); however, the maximum response was attenuated only in SHR6wk. There were significant fibrosis, LVH, and increased LV pressure in SHR6wk compared with any other group, and CZ regressed LVH and LV pressure. Results suggest that early in HT, except for eNO dysfunction, other contractile responses are preserved; however, at 6 weeks there is significant nonendothelial cell dysfunction, and treatment with CZ reverses this nonendothelial dysfunction as well.

Acetylcholine↗

PubMed2002

A case of chorea-acanthocytosis with dysautonomia; quantitative autonomic deficits using CASS.

The purpose of this study was to quantitatively assess cardiovagal, adrenergic and postganglionic sudomotor functions in a patient with chorea-acanthocytosis. We describe a 25-year-old woman with acanthocytosis, lip and tongue biting, chorea like movements and increased levels of serum creatine phosphokinase. The patient presented with orthostatic hypotension. The heart period response to deep breathing was moderately decreased and the quantitative sudomotor axon reflex test (QSART) was mildly abnormal in the lower extremities. The composite autonomic score (CASS) for this patient was 6 points which indicates moderate autonomic failure. Although a few previous reports have described autonomic dysfunction associated with chorea-acanthocytosis and have indicated that impairment is primarily sympathetic, our case study suggests that there is also parasympathetic dysfunction. We conclude that there is widespread autonomic involvement in choreaacanthocytosis and that autonomic studies are useful in monitoring their course.

Adult↗

PubMed2003

Other autonomic neuropathies.

Acquired forms of autonomic neuropathy may be isolated or may coexist with somatic neuropathy. Clinical identification of symptoms and signs in the patient with autonomic dysfunction is crucial in the diagnosis of autonomic neuropathy and its separation from pure autonomic failure or multiple system atrophy. Once an autonomic neuropathy has been identified, several clinical features can be useful in the diagnosis of a specific form of autonomic neuropathy. Other factors, such as the presence of somatic neuropathy and systemic disease, are critical for diagnosis. This article reviews the clinical presentation, diagnosis, pathogenesis, and management of the acquired forms of autonomic neuropathy.

Animals↗

PubMed2004

Noxious chemical stimulation of rat facial mucosa increases intracranial blood flow through a trigemino-parasympathetic reflex--an experimental model for vascular dysfunctions in cluster headache.

Cluster headache is characterized by typical autonomic dysfunctions including facial and intracranial vascular disturbances. Both the trigeminal and the cranial parasympathetic systems may be involved in mediating these dysfunctions. An experimental model was developed in the rat to measure changes in lacrimation and intracranial blood flow following noxious chemical stimulation of facial mucosa. Blood flow was monitored in arteries of the exposed cranial dura mater and the parietal cortex using laser Doppler flowmetry. Capsaicin (0.01-1 mm) applied to oral or nasal mucosa induced increases in dural and cortical blood flow and provoked lacrimation. These responses were blocked by systemic pre-administration of hexamethonium chloride (20 mg/kg). The evoked increases in dural blood flow were also abolished by topical pre-administration of atropine (1 mm) and [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (0.1 mm), a vasoactive intestinal polypeptide (VIP) antagonist, onto the exposed dura mater. We conclude that noxious stimulation of facial mucosa increases intracranial blood flow and lacrimation via a trigemino-parasympathetic reflex. The blood flow responses seem to be mediated by the release of acetylcholine and VIP within the meninges. Similar mechanisms may be involved in the pathogenesis of cluster headache.

Animals↗

PubMed1997

Prediction of arrhythmia risk based on signal-averaged ECG in postinfarction patients.

In patients surviving acute MI, identification of those at high risk for life-threatening ventricular tachyarrhythmias and/or sudden death is of great importance. Numerous strategies based on indices such as the degree of left ventricular dysfunction, complex ventricular arrhythmias, or parameters of autonomic dysfunction have not yet led to an effective identification of the individual patient at risk. During the past decade, many investigators have recorded low amplitude, high frequency components in the terminal QRS complex (so-called late potentials) from patients prone to sustained ventricular tachycardia. The SAECG has been used to predict life-threatening tachyarrhythmias in patients after acute MI and to screen for inducible ventricular tachycardia in patients with unexplained syncope or sustained ventricular tachycardia. This review article describes the most frequently applied methodology and clinical applications of the SAECG in post-MI patients and discusses the usefulness of noninvasive recordings in various other clinical settings.

Arrhythmias, Cardiac↗

PubMed1998

Abnormal vasovagal reaction, autonomic function, and heart rate variability in patients with paroxysmal atrial fibrillation.

The aim of this study was to evaluate the cardiovascular autonomic function and vasovagal reaction in patients with paroxysmal atrial fibrillation without significant structural heart disease. Twenty-eight patients with paroxysmal atrial fibrillation (9 patients were categorized to have autonomic-mediated atrial fibrillation while atrial fibrillation in other patients was nonautonomic mediated) and 19 normal control subjects were recruited. Cardiovascular autonomic function tests included measuring heart rate response to standing, deep breathing, Valsalva maneuver, baroreflex sensitivity, 24-hour heart rate variability, and also head-up tilt test. Compared with normal subjects, no significant autonomic dysfunction was found in patients with autonomic-mediated and nonautonomic-mediated atrial fibrillation. All subjects had negative baseline tilt test. With isoproterenol provocation, six patients developed atrial fibrillation. Four of 9 patients and 3 of 19 patients with autonomic mediated and nonautonomic mediated atrial fibrillation had a positive tilt test respectively, while none occurred in the controls. A significant percentage (32%) of patients with paroxysmal atrial fibrillation had episodes of atrial fibrillation provoked by changes in autonomic tone, although there was no underlying abnormal cardiac autonomic function nor sympathetic-parasympathetic imbalance. A heightened susceptibility to vasovagal cardiovascular response may have important implications on the occurrence and symptomatology of patients with paroxysmal atrial fibrillation.

Adult↗

PubMed2006

Abnormalities in fractal heart rate dynamics in Chagas disease.

BACKGROUND AND METHODS: In order to study fractal HR dynamics in Chagas disease, we performed detrended fluctuation analysis (DFA)-along with analysis of power-law beta slope (beta index) and standard deviation of N-N intervals (SDNN)-in edited and unedited (with ventricular premature beats - VPBs, only in DFA analysis) series of R-R intervals from Holter monitoring of healthy controls (Group 0, n = 27) and Chagas disease patients with left ventricular (LV) ejection fraction >50% (Group 1, n = 137) and with LV ejection fraction <50% (Group 2, n = 23). RESULTS: When analyzed from the edited R-R interval data, the long-term scaling exponent alpha(2) is altered both among the Chagas patients with and without LV dysfunction. The short-term scaling exponent alpha(1) was higher in Group 1 Chagas patients as compared to controls (P < 0.01) and did not differ between Group 2 and controls. In unedited R-R interval series, alpha(1) was significantly reduced in Group 2 Chagas patients (0.55 +/- 0.002) as compared to controls (0.90 +/- 0.002) and Group 1 (0.91 +/- 0.003) (P < 0.001), but did not differ between Group 1 and controls. Similarly alpha(2) was lower in Group 2 compared to other groups (P < 0.001). SDNN did not differ between the groups, but the beta index derived from 1/f model was reduced both in Group 1 and 2 Chagas patients as compared to controls (P < 0.01). There was strong correlation (rs = 0.82; P < 0.001) between the beta and alpha(2) index from edited series. There was an inverse correlation (rs =-0.63, P < 0.01) between the number of VPBs and alpha(1) index of unedited series. CONCLUSIONS: The long-term fractal HR dynamics altered in chagasic patients with and without LV dysfunction could be an early sign of autonomic dysfunction. Patients with impaired LV function show marked alterations in short-term fractal HR dynamics toward more random behavior, mainly due to frequent ectopy. Prospective studies are necessary to define the value of these indices as predictors of death in Chagas disease.

Adult↗

PubMed1986

Are cardiovascular reflexes more commonly impaired in patients with bronchial carcinoma?

Non-invasive tests of cardiovascular autonomic function were performed in 69 patients with histologically proved bronchial carcinoma and the results compared with those obtained in a group of age and sex matched controls. Only two patients were under 50 years of age, and with the exception of the heart rate response to deep breathing the tests performed have no accepted normal ranges in patients of this age. None of the patients had features of florid, disabling autonomic neuropathy. All the tests of autonomic function showed declining performance with age but in addition there were significant differences in the results when the two groups were compared. In the group with carcinoma the resting heart rate was higher (p less than 0.05), the resting supine blood pressure lower (p less than 0.01), and the postural fall in blood pressure greater (p less than 0.01). Test results were not related to tumour histology, the presence of finger clubbing, drug history, or symptoms suggestive of autonomic dysfunction. Abnormal responses in tests of cardiovascular autonomic function are commonly found in elderly patients but bronchial carcinoma appears to have an additional effect. The precise mechanism of this effect remains a matter for speculation.

Adult↗

PubMed1997

Influence of autonomic neuropathy of different severities on the hypercapnic drive to breathing in diabetic patients.

To investigate the effects of the autonomic nervous system on control of breathing, the neuromuscular (mouth occlusion pressure at 0.1 s after onset of inspiration [P0.1]) and ventilatory (minute ventilation [VE]) response to progressive hyperoxic hypercapnia was assessed in diabetic patients with autonomic dysfunction of different severity. Eighteen diabetics with autonomic neuropathy, nine with parasympathetic damage (DANp), and nine with parasympathetic and sympathetic damage (DANp+s), as indicated by marked postural hypotension, low increment of diastolic BP during sustained handgrip, and lowest resting catecholamine plasma levels, were studied together with a group of 10 diabetic patients without autonomic neuropathy (D) and a group of 10 normal subjects (C). All subjects had pulmonary function tests, including maximal voluntary ventilation and diffusion of carbon monoxide, measurements of respiratory muscle strength as maximal inspiratory mouth pressure (MIP) and maximal expiratory mouth pressure (MEP), and a CO2 rebreathing test (Read's method). Although in the normal range, lung volumes and FEV1 and forced expiratory flows were lower in the DANp and DANp+s groups than in the D and C groups, MIP and MEP were similar among C and diabetic groups, as well as resting P0.1, VE, tidal volume (VT), and respiratory rate (RR). The slope of the linear relationship between P0.1 and end-tidal PCO2 (PETCO2) was higher in DANp+s (0.63+/-0.07 cm H2O/mm Hg) than in C (0.45+/-0.06 cm H2O/mm Hg; p<0.05) and three times greater in DANp+s than in D (0.26+/-0.03 cm H2O/mm Hg; p<0.001) and DANp (0.24+/-0.03 cm H2O/mm Hg; p<0.001), who in turn showed a lower deltaP0.1/deltaPETCO2 than C. The VE increase with increasing PETCO2 was greater in DANp+s (3.70+/-0.85 L/min/mm Hg) than in DANp (2.13+/-0.20 L/min/mm Hg; p<0.05) and D (2.37+/-0.40 L/min/mm Hg; p=0.07), but not significantly higher from that of C (3.17+/-0.36 L/min/mm Hg). No differences were found for deltaVT/deltaPETCO2 among the groups, whereas the deltaRR/deltaPETCO2 relationship was steeper in DANp+s than in DANp (p<0.05) and D (p=0.055). These data reflect a depressed CO2 response both in D and DANp. The presumable decrease of the sympathetic nerve traffic in DANp+s appears to reverse this abnormality. DANp+s, however, exhibit an enhanced CO2 neuromuscular response even in respect to C, suggesting that the sympathetic nervous system might modulate the output of the respiratory centers to hypercapnic stimulus.

Adult↗