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 effects of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep were compared in six patients with chronic obstructive lung disease and carbon dioxide retention. Patients received 1.5 mg/kg almitrine (a peripheral chemoreceptor stimulant), 100 mg of medroxyprogesterone (a central respiratory stimulant), or matched placebo daily for 15 days in random order in a crossover trial. When subjects were awake almitrine increased the ventilatory response to hypoxia and increased arterial oxygen tension (PaO2) to a greater extent than medroxyprogesterone, whereas medroxyprogesterone augmented the ventilatory response to hypercapnia and decreased arterial carbon dioxide tension (PaCO2) to a greater extent than almitrine. Neither drug influenced sleep architecture significantly, except that medroxyprogesterone increased the number of arousals. Almitrine had a more favourable effect than placebo on oxygenation as estimated from arterial oxygen saturation (SaO2) during the different stages of sleep, the number of episodes of hypoxaemia, and the amount of time that SaO2 was below 80%. The only change with medroxyprogesterone by comparison with placebo was a decrease in the number of hypoxaemic episodes. It is concluded that both active drugs improved blood gases during wakefulness, but that 1.5 mg/kg of almitrine is superior to 100 mg of medroxyprogesterone in improving SaO2 during sleep.
Thorax 1990 Sep
PMID:Comparison of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep in patients with chronic obstructive lung disease. 214 54

The effects of chronic respiratory failure (hypoxia and hypercapnia) on the contractile properties of cardiac muscle are not established. A study was performed of the isometric contractile properties of isolated papillary muscle removed from rats exposed in a normobaric environmental chamber to 28 days of hypoxia (fractional inspired oxygen (FIO2) 10%, fractional inspired carbon dioxide (FICO2) less than 1%), hypercapnia (FIO2 21%, FICO2 5%), and hypoxia with hypercapnia (FIO2 10%, FICO2 5%). Rats exposed to both hypoxia and hypoxia with hypercapnia developed selective right ventricular hypertrophy. Exposure to hypercapnia alone did not alter right ventricular weight. No change in right ventricular papillary muscle contractility per unit muscle mass was observed as measured by maximum active tension, maximum rate of rise or fall of tension, or time to peak tension. Rat cardiac muscle adapts successfully to the altered acid-base environment and increased work load associated with prolonged exposure to hypoxia and mild hypercapnia.
Thorax 1989 Oct
PMID:Contractility of papillary muscle from rats exposed to 28 days of hypoxia, hypercapnia, and hypoxia with hypercapnia. 259 23

The ventilatory response to isocapnic progressive hypoxia and hyperoxic progressive hypercapnia in 24 diabetic patients were compared with those of sex and age matched normal control subjects. The heart rate response to hypoxia was also measured in both groups. In diabetic patients the ventilatory and heart rate responses to hypoxia were significantly lower than those in the control group (0.10 v 0.24 l/min/% fall/m2 and 0.5 l v 1.27 beats/min/% fall respectively). The ventilatory response to hypercapnia was significantly higher (1.09 v 0.76 l/min/mm Hg/m2) in the diabetic patients. There was a significant correlation between the hypoxic ventilatory response and the heart rate response in diabetic patients (r = 0.56), but not in the control group (r = 0.28). In addition, both the ventilatory and the heart rate responses to hypoxia in diabetic patients had weak but significant correlations with the heart rate variation during deep breathing. It is concluded that the ventilatory and heart rate responses to hypoxia in diabetic patients are impaired, whereas the ventilatory response to hypercapnia is well preserved.
Thorax 1989 Apr
PMID:Ventilatory and heart rate responses to hypoxia and hypercapnia in patients with diabetes mellitus. 276 26

Previous studies have shown that some patients with chronic obstructive lung disease and hypercapnia will respond to medroxyprogesterone with improvement in arterial blood gases. The exact mechanism of this effect is unclear but it is presumed to be a result of ventilatory stimulation. To determine whether the ability to correct arterial blood gas abnormalities by voluntary hyperventilation would predict a subsequent favourable response to progesterone, we studied 11 subjects with chronic obstructive lung disease and chronic hypercapnia. Five subjects had chronic obstructive lung disease of moderate severity with mean (SE) FEV1 1.8 (0.34) 1 maximum voluntary ventilation (MVV) 40.4 (7.16) 1/min-1, arterial oxygen tension (Pao2) 53.8 (2.40 mm Hg, and arterial carbon dioxide tension Paco2) 49.6 (3.91) mm Hg, and were able to normalise their blood gas tensions during voluntary hyperventilation (Pao2 85.4 (8.01) mm Hg; Paco2 32.8 (3.43) mm Hg). Six subjects had severe chronic obstructive lung disease with FEV1 0.77 (0.12) 1, MVV 19 (3.09) 1/min-1, Pao2 60.0 (2.89) mm Hg and Paco2 50.5 (1.38) mm Hg, and they could not significantly alter their blood gases with voluntary hyperventilation (Pao2 62.5 (3.19) mm Hg, Paco2 49.7 (1.84) mm Hg). The groups were similar in age, height, weight, and resting Pao2 and Paco2. Each subject received one month of oral placebo and one month of medroxyprogesterone acetate (Provera). 20 mg orally thrice daily, given in a randomised, double blind fashion. The groups responded similarly with a significantly higher Pao2 and lower Paco2 while having medroxyprogesterone acetate than while having placebo. Two patients with polycythaemia showed a reduction in haemoglobin concentration while taking progesterone. It is concluded that the response to medroxyprogesterone is not predictable from spirometric or blood gas changes after voluntary hyperventilation.
Thorax 1986 Aug
PMID:Oral progesterone treatment in chronic obstructive lung disease: failure of voluntary hyperventilation to predict response. 294 45

The effect of a single dose of diazepam on sleep and respiration was studied in nine patients with chronic airflow obstruction with moderate arterial hypoxaemia but no hypercapnia. Diazepam improved sleep duration without exacerbating nocturnal hypoxaemia and there was no change in the number of apnoeic events after a single 5 mg dose at night.
Thorax 1988 Sep
PMID:Effect of diazepam on sleep in patients with chronic airflow obstruction. 305 77

Thirty six patients previously treated for pulmonary tuberculosis by thoracoplasty were studied to determine the prevalence and effect of airflow obstruction. The mean (SD) FEV1 was 1.3 (0.65) 1 and the mean forced expiratory ratio (FER) 64% (12%). FEV1 was less than predicted in every patient whereas FER was less than predicted in 30, being below the lower 98th percentile in 15 (42%). In the 18 patients who complained of breathlessness the means of the standardised residuals (SR) for FEV1, peak expiratory flow (PEF), and FER were significantly lower and that for residual volume/total lung capacity (RV/TLC) significantly higher than those for the 18 patients who were not breathless (all p less than 0.0001). There was no difference in the smoking history of the two groups. Only three of the 23 patients in whom reversibility of airflow obstruction was assessed showed a greater than 25% increase in PEF. None showed an increase in FEV1 of greater than 15%. The 18 who were breathless had significantly lower values of arterial oxygen tension (PaO2) and higher values of arterial carbon dioxide tension (PaCO2) (p less than 0.0001). Thirteen of these patients were in chronic respiratory failure (PaO2 less than 8.0 kPa or PaCO2 greater than 5.9 kPa, or both) compared with only one of the 18 who were not breathless. The indices correlating best with PaO2 and PaCO2 were SR FEV1 and SR PEF respectively. SR FEV1 accounted for 34% of the variance in PaO2 and SR PEF for 29% of the variance in PaCO2. Airflow obstruction has been found to be common in patients with a thoracoplasty and to be associated with hypoxia and hypercapnia.
Thorax 1987 May
PMID:Importance of airflow obstruction after thoracoplasty. 366 Feb 88

The respiratory effects of intravenously infused almitrine were evaluated in healthy volunteers. In the dose range 0.25-1.0 mg/kg/hour it caused large and dose-dependent increases in hypoxic chemosensitivity, which were longlasting and more persistent than the drug's retention in the plasma. Increases in sensitivity to hypercapnia were much less and were detected only when the plasma almitrine exceeded 200 ng/ml. Small increases in resting ventilation and metabolic rate with a decrease in mixed venous carbon dioxide tension occurred only at the highest infusion rate. The findings accord with an action of almitrine in the peripheral chemoreceptors, which may be of therapeutic value in managing some cases of respiratory failure.
Thorax 1983 Mar
PMID:Increased respiratory chemosensitivity induced by infusing almitrine intravenously in healthy man. 613 50

From 1967 to 1972 12 patients were operated on for emphysematous bullae in the Liverpool regional cardiothoracic centre. The patient with the poorest lung function died in the immediate postoperative period but the remainder survived for more than five years. All but one of the survivors showed evidence of benefit three to six months after surgery and all those not retired returned to full-time employment for at least five years. Nine patients were reviewed 5-10 years after surgery. These all reported a gradual return of dyspnoea, which was matched by a falling one-second forced expiratory volume (FEV1) (mean fall 82 ml a year); but five were still maintaining some of their postoperative improvement. When mean preoperative lung function values were compared with the values obtained 5-10 years later there was still a significant improvement in forced vital capacity; but FEV1, residual volume, transfer coefficient, and arterial oxygen and carbon dioxide tensions were unchanged. Chest radiographs showed no new bullae or (except in one case) any increase in size of pre-existing bullae. We conclude that the removal of large emphysematous bullae did not hasten the progress of the underlying emphysema and that in most patients some benefit lasted for more than five years after the operation. Patients treated by lobectomy fared at least as well as those treated by bullectomy alone. It may be relevant to the relatively good progress of patients in this series that only three had suffered from chronic bronchitis before operation or smoked after operation, all but two had bullae occupying half or more of one hemithorax, and none had hypercapnia.
Thorax 1983 Feb
PMID:Surgical treatment of emphysematous bullae: late outcome. 640 36

We studied 53 patients with proximal myopathy to determine at what level of muscle weakness hypercapnic respiratory failure is likely, and which tests of pulmonary function or respiratory muscle strength would best suggest this development. Respiratory muscle strength was determined from maximal static efforts and in half the patients, both inspiratory and expiratory muscle strengths were less than 50% of normal. In the 37 patients without lung disease respiratory muscle weakness was accompanied by significant decreases in vital capacity, total lung capacity, and maximum voluntary ventilation; by significant increases in residual volume and arterial carbon dioxide tension (PaCO2); and greater likelihood of dependence on ventilators, atelectasis, and pneumonia. Hypercapnia was particularly likely when respiratory muscle strength was less than 30% of normal in uncomplicated myopathy, and when vital capacity was less than 55% of the predicted value in any patient.
Thorax 1983 Aug
PMID:Respiratory muscle and pulmonary function in polymyositis and other proximal myopathies. 641 85

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.
Thorax 1984 Jul
PMID:Respiratory responses of diabetics to hypoxia, hypercapnia, and exercise. 643 27


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