Increased bronchial reactivity to histamine in diabetic autonomic neuropathy

1987 ◽  
Vol 73 (4) ◽  
pp. 401-405 ◽  
Author(s):  
George B. Rhind ◽  
Grahame A. Gould ◽  
David J. Ewing ◽  
Basil F. Clarke ◽  
Neil J. Douglas
Keyword(s):  
Autonomic Neuropathy ◽  
Maximum Concentration ◽  
Vital Capacity ◽  
Forced Expiratory Volume ◽  
Diabetic Autonomic Neuropathy ◽  
The Other ◽  
Autonomic Nerves ◽  
Diabetic Patients ◽  
Maximal Flow ◽  
Bronchial Reactivity

1. Twelve male diabetic patients inhaled nebulized histamine in doubling concentrations from 0.03 mg/ml to 32 mg/ml until they reached the maximum concentration or until their forced expiratory volume in 1 s (FEV1.0) fell by at least 20%. Six had evidence of severe autonomic neuropathy (DAN), while the other six did not. 2. More of the DAN group decreased their FEV1.0 on histamine inhalation by at least 20% (P < 0.02) and more of them decreased their maximal flow at 50% vital capacity by at least 20% than those in the group without DAN (P < 0.05). 3. The fall in FEV1.0 and in maximal flow at 50% of vital capacity was greater (P < 0.05) in the DAN group than in the group without DAN. 4. This suggests that diabetic patients with autonomic neuropathy have increased bronchial reactivity to histamine. This could either be due to differential damage of the respiratory autonomic nerves or, alternatively, to denervation hypersensitivity.

Interaction of inhaled LTC4 with histamine and PGD2 on airway caliber in asthma

1989 ◽  
Vol 66 (1) ◽  
pp. 304-312 ◽  
Author(s):  
G. D. Phillips ◽  
S. T. Holgate
Keyword(s):  
Time Course ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Forced Expiratory Volume ◽  
Maximal Flow ◽  
Lung Capacity ◽  
Airway Caliber ◽  
Relevant Interaction

To investigate possible mediator interaction in asthma, the effect of inhaled leukotriene (LT) C4 on bronchoconstriction provoked by histamine and prostaglandin (PG) D2 was studied in nine asthmatic subjects. The provocation doses of histamine, PGD2, and LTC4 required to produce a 12.5% decrease in baseline forced expiratory volume in 1 s (FEV1, PD12.5) and to further this fall to 25% (PD25–12.5) were determined. On three subsequent occasions, subjects inhaled either the PD12.5 LTC4 plus vehicle or vehicle plus the PD25–12.5 of either histamine or PGD2, and FEV1 and maximal flow at 70% of vital capacity below total lung capacity after a forced partial expiratory maneuver (Vp30) followed for 45 min. From these results, predicted time-course curves for LTC4 with histamine and LTC4 with PGD2 were calculated. On two final occasions, airway caliber was followed for 45 min after inhalation of the PD12.5 LTC4 followed by the PD25–12.5 of either histamine or PGD2. During the first 9 min after LTC4-histamine and LTC4-PGD2, the decreases in airway caliber were greater than the calculated predicted response. This interaction, although small, was significant with LTC4-PGD2 for both FEV1 (P = 0.01) and Vp30 (P less than 0.05) and with LTC4-histamine for Vp30 (P less than 0.05) but not for FEV1 (P less than 0.05). We conclude that inhaled LTC4 interacts synergistically with histamine and PGD2 and that this effect, although small, may be a relevant interaction in asthma.

scholarly journals Rehabilitation for diabetic patients with diabetic autonomic neuropathy

2014 ◽  
Vol 5 (1) ◽  
pp. 52-57
Author(s):  
Takuo Nomura ◽  
Fuminari Asada ◽  
Hiroshi Kondo ◽  
Masayuki Ueno
Keyword(s):  
Autonomic Neuropathy ◽  
Diabetic Autonomic Neuropathy ◽  
Diabetic Patients

scholarly journals Pupillary responses to single and sinusoidal light stimuli in diabetic patients

2009 ◽  
Vol 1 (1) ◽  
pp. 19 ◽  
Author(s):  
Wolfgang H. Zangemeister ◽  
Thilo Gronow ◽  
Ulrich Grzyska
Keyword(s):  
Autonomic Neuropathy ◽  
Pupillary Light Reflex ◽  
Diabetic Autonomic Neuropathy ◽  
Characteristic Change ◽  
Diabetic Patients ◽  
Frequency Content ◽  
Light Reflex ◽  
Pupillary Light ◽  
Pupillary Responses ◽  
Short Time

We examined effects of diabetes mellitus (DM) on the pupillary light reflex (PLR). Phasic pupillary response to a single light stimulus (200 ms) (pPLR) and to continuous sinusoidal stimuli with four different frequencies (0.1, 0.3, 0.7, 1.3Hz) (cPLR) were examined in 52 DM patients and 21 control subjects. We asked: does recording and frequency analysis of cPLR together with short time fourier [STFT] analysis of pPLR differentiate better between DM patients and normal subjects than pPLR only? Initial pupil diameter was significantly decreased in the DM group. For pPLR. maximal contraction velocity (Vmax), Vmax of redilation 1, reflex-amplitude and pPLR latency were significantly reduced in those patients who also showed signs of diabetic autonomic neuropathy (DNP). Tests of dynamic pupillary light reflex (cPLR) revealed that all DM patients had a significantly reduced gain at lower frequencies. Pupil phase lag was greater at 0.1 and 0.3Hz and smaller at 0.7 and 1.3 Hz in the DNP group (p<0.001). Comparison of single pPLR recordings of 5 DNP patients with 5 subjects using short time fast fourier (STFT) analysis revealed a characteristic change from low frequency content in healthy subjects to high frequency content in DNP patients. Significant changes in the PLR in DM can be found only when symptoms of autonomic neuropathy have been shown. Both sympathetic and the parasympathetic nervous systems are affected by diabetic autonomic neuropathy. Only recording of cPLR , together with STFT of pPLR can identify significant pathological deficits of pupillary control in single cases.

Preservation of the Hypoxic Drive to Breathing in Diabetic Autonomic Neuropathy

1982 ◽  
Vol 63 (1) ◽  
pp. 17-22 ◽  
Author(s):  
P. M. A. Calverley ◽  
D. J. Ewing ◽  
I. W. Campbell ◽  
P. K. Wraith ◽  
H. M. Brash ◽  
...  
Keyword(s):  
Heart Rate ◽  
Autonomic Neuropathy ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Diabetic Autonomic Neuropathy ◽  
Co2 Production ◽  
Diabetic Patients ◽  
Normal Range ◽  
Peripheral Chemoreceptors ◽  
Carotid Chemoreceptors

1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia () during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN−). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients ( in DAN+ patients = −0·9 ± 0·2 litre min−1 kPa−1; in DAN− patients = −1·2 ± 0·6 litres min−1 kPa−1) even allowing for differences in the level of exercise achieved (CO2 production in DAN+ patients = 743 ± 103 ml/min; CO2 production in DAN– patients = 800 ± 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly (P < 0·05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients.

Diabetic Autonomic Neuropathy

1999 ◽  
Vol 12 (2) ◽  
pp. 142-154
Author(s):  
Roy C. Parish
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Drug Therapy ◽  
Autonomic Neuropathy ◽  
Cardiac Arrhythmias ◽  
Diabetic Autonomic Neuropathy ◽  
Diabetic Patients ◽  
Specific Information ◽  
Autonomic Nervous ◽  
Increased Risk

Diabetic autonomic neuropathy (DAN) occurs in approximately half of Caucasian patients with diabetes and perhaps three-fourths of black diabetic patients. This may be asymptomatic for several years, but the majority of patients with DAN eventually exhibit symptoms of diarrhea, cardiac arrhythmias, sexual dysfunction, and abnormal sweating. Prolonged hyperglycemia results in damage to the autonomic nervous system (ANS), particularly the vagus nerve and other parts of the parasympathetic division. DAN is associated with increased risk of sudden death, high-risk cardiac arrhythmias, myocardial infarction, and death from other causes. Objective testing of autonomic nervous system function yields specific information that affects treatment decisions. Drug therapy can effect improvements in ANS function and reduce these risks. Complications of diabetes that result from ANS dysfunction can be partly reversed or their progress can be slowed by appropriate drug therapy. Features, implications, and therapy of the most common complications resulting from DAN are reviewed, and suggestions for pharmacist involvement in the care of these difficult patients are offered.

scholarly journals Impaired hypoxic ventilatory drive induced by diabetic autonomic neuropathy, a cause of misdiagnosed severe cardiac events: brief report of two cases

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Louis Schubert ◽  
Suzanne Laroche ◽  
Agnès Hartemann ◽  
Olivier Bourron ◽  
Franck Phan
Keyword(s):  
Respiratory Failure ◽  
Autonomic Neuropathy ◽  
Clinical Signs ◽  
Diabetic Autonomic Neuropathy ◽  
Cardiac Autonomic Neuropathy ◽  
Diabetic Patients ◽  
Cardiac Events ◽  
Cardiorespiratory Arrest ◽  
Ventilatory Drive ◽  
Clinical Cases

Abstract Background Sudden cardiac deaths are twice more frequent in diabetic patients with cardiac autonomic neuropathy. Sudden cardiac death etiologies remain unclear and no recommendations are made to identify factors associated with cardiorespiratory arrest in diabetic patients. We hypothesized, from two clinical cases, that impaired hypoxic ventilatory drive, induced by diabetic autonomic neuropathy, is a cause of misdiagnosed severe cardiac events. Case presentation We describe the cases of two patients with isolated low blood saturation on pulse oximeter during the systematic nurse check-up (77% and 85% respectively) contrasting with the absence of any complaint such as dyspnea, polypnea or other respiratory insufficiency signs observed during the clinical examination. Arterial blood gas measurements subsequently confirmed that blood oxygen saturation was low and both patients were indeed hypoxemic. Patient 1 suffered from vascular overload complicated by cardiac arrest caused by hypoxemia in light of the quick recovery observed after ventilation. Pulmonary edema was diagnosed in patient 2. The common denominator of these 2 cases described in this brief report is the absence of respiratory failure clinical signs contrasting with the presence of confirmed hypoxemia. Also, in both cases, such absence of precursory signs seems to be induced by an impaired ventilatory drive to hypoxemia. This appears to be related to the autonomic diabetic neuropathy encountered in those 2 patients. Conclusions Therefore, we describe, in this brief report, cardiac autonomic neuropathy as a cause of impaired hypoxic ventilatory drive involved in severe acute cardiorespiratory events in two type 1 diabetic patients. We assume that altered response to hypoxemia due to cardiac autonomic neuropathy and non-functional central neurological breathing command could play a key role in sudden deaths among diabetic patients. An important point is that hypoxemia can be easily missed since no clinical signs of respiratory failure are reported in these two clinical cases. Systematic screening of cardiac autonomic neuropathy in diabetic patients and proactive detection of impaired hypoxic ventilatory drive for early management (e.g. treatment of hypoxemia) should be systematically undertaken in diabetic patients to prevent its dramatic consequences such as cardiorespiratory arrest and death.

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