Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ventilatory control system was evaluated in a group of 40 diabetic patients (20 with autonomic neuropathy (AN), and 20 without autonomic neuropathy) and 20 controls. The ventilatory increase in response to transient hypoxia was less in diabetics without AN than in controls, but even weaker in diabetics with AN. This pattern was repeated in the ventilatory response to hypercapnia. There was no correlation between the presence of abnormal respiratory responses and the duration of diabetes.
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PMID:Ventilatory control in diabetes mellitus. 405 61

The respiratory responses of 52 diabetics and 65 non-diabetic controls to hypoxia, hypercapnia, and exercise were studied. Twenty five per cent of the diabetics had evidence of impaired sensitivity to hypoxia or decreased ventilatory response to hypercapnia, while 7% of the diabetics who performed the exercise tests had an abnormal pattern of respiration during exercise; 33% of the diabetics who performed all three tests of respiratory reflex action had at least one abnormal test response. There was no correlation between the presence of an abnormal respiratory response and the presence of clinical diabetic complications. Abnormal respiratory reflexes could not be predicted from the results of the "routine" pulmonary function tests. The possibility that the abnormal respiratory responses were due to autonomic neuropathy is discussed.
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PMID:Respiratory responses of diabetics to hypoxia, hypercapnia, and exercise. 643 27

To investigate one suggested cause of unexplained deaths of diabetic patients with autonomic neuropathy, ventilatory responses to progressive hypoxemia and to progressive hypercarbia were compared among two groups of diabetic patients, with and without autonomic neuropathy, and a group of normal control subjects. Hypoxemia was induced gradually under isocapnic conditions and the arterial oxygen saturation was reduced to below 75%. In a separate test the end tidal CO2 was increased gradually to 55 mm Hg in subjects who could tolerate this degree of hypercarbia. The ventilatory responses to hypoxemia and to hypercarbia did not differ among groups nor did age, duration of diabetes, or presence of proliferative retinopathy and nephropathy have a significant effect on the ventilatory responses of diabetics. The authors conclude that defective ventilatory responses to hypoxemia or hypercarbia are not associated with the sudden unexplained deaths in diabetics with autonomic neuropathy.
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PMID:Autonomic neuropathy and the ventilatory responses of diabetics to progressive hypoxemia and hypercarbia. 716 May 39

The impact of autonomic neuropathy (common in patients on haemodialysis) on ventilatory response to hypercapnia has been studied. We investigated cardiac reflex tests in 20 patients on chronic haemodialysis (8 patients were found with and 12 without neuropathy of the autonomic nervous system). Using the hyperoxic CO2-rebreathing method (according to Read), we tested the above-mentioned two groups of patients and compared them with 14 healthy control subjects. Accumulation of CO2 in blood with hyperoxic CO2 rebreathing stimulates central chemoreceptors, and therefore causes a progressive rise in minute ventilation. In patients with autonomic neuropathy (n = 8), ventilatory response to increasing pCO2 was significantly lower than that in the controls (1.7 +/- 0.3 versus 3.2 +/- 0.5 l/min/mmHg, P < 0.001). On the other hand ventilatory response in patients without autonomic damage (n = 12) showed no significant difference when compared to controls (3.1 +/- 0.8 l/min/mmHg). There were no differences in lung function, arterial blood gas analysis, blood chemistry, duration on dialysis, and demographic data when comparing the patients with and those without autonomic damage. Our analysis shows different patterns of ventilatory response to increasing pCO2 in patients on haemodialysis. Autonomic neuropathy has to be considered when rebreathing tests are interpreted. The clinical relevance of these findings needs further investigation.
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PMID:Effect of autonomic neuropathy on ventilatory response to progressive hypercapnia in dialysis patients. 756 11

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.
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PMID:Influence of autonomic neuropathy of different severities on the hypercapnic drive to breathing in diabetic patients. 922 70

Because abnormalities in cerebrovascular reactivity (CVR) in subjects with long-term diabetes could partly be ascribed to autonomic neuropathy and related to central chemosensitivity, CVR and the respiratory drive output during progressive hypercapnia were studied in 15 diabetic patients without (DAN-) and 30 with autonomic neuropathy (DAN+), of whom 15 had postural hypotension (PH) (DAN+PH+) and 15 did not (DAN+PH-), and in 15 control (C) subjects. During CO(2) rebreathing, changes in occlusion pressure and minute ventilation were assessed, and seven subjects in each group had simultaneous measurements of the middle cerebral artery mean blood velocity (MCAV) by transcranial Doppler. The respiratory output to CO(2) was greater in DAN+PH+ than in DAN+PH- and DAN- (P < 0.01), whereas a reduced chemosensitivity was found in DAN+PH- (P < 0.05 vs. C). MCAV increased linearly with the end-tidal PCO(2) (PET(CO(2))) in DAN+PH- but less than in C and DAN- (P < 0.01). In contrast, DAN+PH+ showed an exponential increment in MCAV with PET(CO(2)) mainly >55 Torr. Thus CVR was lower in DAN+ than in C at PET(CO(2)) <55 Torr (P < 0.01), whereas it was greater in DAN+PH+ than in DAN+PH- (P < 0.01) and DAN- (P < 0.05) at PET(CO(2)) >55 Torr. CVR and occlusion pressure during hypercapnia were correlated only in DAN+ (r = 0.91, P < 0.001). We conclude that, in diabetic patients with autonomic neuropathy, CVR to CO(2) is reduced or increased according to the severity of dysautonomy and intensity of stimulus and appears to modulate the hypercapnic respiratory drive.
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PMID:Cerebrovascular reactivity and hypercapnic respiratory drive in diabetic autonomic neuropathy. 1118 97

Familial dysautonomia (Riley-Day syndrome, hereditary sensory and autonomic neuropathy type III) is a rare autosomal recessive disease characterized by impaired development of primary sensory and autonomic neurons resulting in a severe neurological phenotype, which includes arterial baroreflex and chemoreflex failure with high frequency of sleep-disordered breathing and sudden death during sleep. Although a rare disease, familial dysautonomia represents a unique template to study the interactions between sleep-disordered breathing and abnormal chemo- and baroreflex function. In patients with familial dysautonomia, ventilatory responses to hypercapnia are reduced, and to hypoxia are almost absent. In response to hypoxia, these patients develop paradoxical hypoventilation, hypotension, bradycardia, and potentially, death. Impaired ventilatory control due to chemoreflex failure acquires special relevance during sleep when conscious control of respiration withdraws. Overall, almost all adult (85%) and pediatric (95%) patients have some degree of sleep-disordered breathing. Obstructive apnea events are more frequent in adults, whereas central apnea events are more severe and frequent in children. The annual incidence rate of sudden death during sleep in patients with familial dysautonomia is 3.4 per 1000 person-year, compared to 0.5-1 per 1000 person-year of sudden unexpected death in epilepsy. This review summarizes recent developments in the understanding of sleep-disordered breathing in patients with familial dysautonomia, the risk factors for sudden death during sleep, and the specific interventions that could prevent it.
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PMID:Chemoreflex failure and sleep-disordered breathing in familial dysautonomia: Implications for sudden death during sleep. 3089 Mar 43