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Query: HUMANGGP:003739 (CO2)
 48,959 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of carbonic anhydrase B and C isozymes in human red cells were determined using a quantitative immunological technique in patients with chronic obstructive lung disease. A significant increase in the level of carbonic anhydrase B was observed in these patients, while the level of carbonic anhydrase C did not change substantially. Positive correlations were found between the level of carbonic anhydrase B and arterial CO2 tension and plasma HCO3 concentration. A negative correlation was observed between the levels of carbonic anhydrase B and blood pH. These findings suggest that the synthesis or degradation of carbonic anhydrase B isozyme is affected by arterial CO2 tension or plasma HC03 concentration. The clinical significance was also discussed in relation to these isozyme levels in red cell.
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PMID:Human erythrocyte carbonic anhydrase B and C in chronic obstructive lung disease. 0 69

In 20 patients with chronic hypoxemia due to chronic obstructive pulmonary disease, we measured responses to CO2 and hypoxia in terms of ventilation and P0.1, the pressure generated by the respiratory muscles during the first 0.1 s of inspiratory effort against a closed airway at functional residual capacity. These responses were compared to those of a control group of 17 patients with similar ventilatory abnormality but without hypoxemia. Hypoxemic patients demonstrated significantly less response to hypoxia than did control subjects in terms of both ventilation and P0.1 The decreased hypoxic response might be analogous to that reported in high altitude dwellers and patients with cyanotic congenital heart disease. Ventilatory responses to CO2 were depressed in hypoxemic patients, but P0.1 responses were not significantly decreased. While breathing at rest with arterial O2 saturation of 95 per cent, hypoxemic patients demonstrated the same minute ventilation as control subjects, but tidal volume was smaller, inspiratory duration was shorter, and breathing frequency was slightly higher. This breathing pattern appeared to be independent of whether or not these patients retained CO2.
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PMID:Ventilatory control in patients with hypoxemia due to obstructive lung disease. 3 89

Nitroglycerin was administered to a group of 11 patients with chronic obstructive pulmonary disease in a dose of 0.4 mg sublingually. Arterial blood gases and blood pressure and pulse were measured at 5-min intervals for 30 min after nitroglycerin. There was a slight decrease in arterial O2 tension for the duration of the study; the maximal change was from a mean pre-nitroglycerin value of 53.5 mm Hg to 50.3 mm Hg at 20 min. In addition, there was a slight reduction in arterial CO2 tension and bicarbonate for 25 min. It is postulated that decreased O2 transport (due to increased hypoxemia and probably decreased cardiac output) plus hypocapnia were a sufficient stimulus to raise blood lactate. It is recommended that in patients receiving nitroglycerin who have obstructive airway disease, attention be directed toward the effect on arterial blood gases.
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PMID:The effect of nitroglycerin in gas exchange on chronic obstructive pulmonary disease. 23 14

During CO2 rebreathing, we measured the pressures generated at the mouth and in the esophagus during the first 0.1 sec of inspiratory effort against a closed airway in 6 normal subjects and 6 patients with chronic obstructive lung disease. Normal subjects showed similar reponses to CO2 in terms of both mouth pressure and esophageal pressure. Patients' responses at the mouth to CO2 were decreased compared to those of normal subjects, but the responses in the esophagus were not significantly different. The patients demonstrated a greater response of occlusion pressure measured in the esophagus than at the mouth. In patients with altered mechanical properties of the lung, the change in mouth occlusion pressure might be influenced by problems of equalization of pressure within the airways due to unequal time constants, by problems of regional differences in pressure gradients over the pleural surface, or both. Esophageal pressure during airway occlusion 100 msec after the onset of inspiration may be better measure of respiratory drive than mouth pressure in patients with intrinsic increase of airway resistance.
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PMID:Diffference between mouth and esophageal occlusion pressure during CO2 rebreathing in chronic obstructive pulmonary disease. 36 9

In a previously reported study of a group of normal subjects, large decreases in arterial O2 tension (PaO2) of as much as 37 mm Hg were measured during the first 90 sec of slow stair-climbing exercise (chosen as a common daily exertion). This study reports the changes in PaO2, arterial CO2 tension (PaCO2), and ventilation in 7 patients with chronic obstructive pulmonary disease and resting hypoxemia during the first 90 sec of similar exercise. The patient group showed significantly smaller unsteady-state decreases in PaO2 starting from a smaller resting value (patient group, 72 +/- 2.6 mm Hg, mean +/- SE; normal group, 92 +/- mm Hg; P less than 0.001) and decreasing to a similar smallest value (patient group, 58 +/- 3.8 mm Hg; normal group, 65 +/- 3.4 Hg; P greater than 0.05). PaCO2 tended to oscillate around the resting value in both the patient group and the normal group, and the rates of increase in ventilation in the 2 groups were similar. The physiologic processes that could limit the unsteady-state decrease in PaCO2 in the patient group are analyzed, the analysis suggesting that a slower rate of increase in tissue consumption of O2 is most likely to account for the smaller decrease in PaO2.
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PMID:Arterial blood gas tension changes at the start of exercise in chronic obstructive pulmonary disease. 43 94

In chronic obstructive pulmonary disease (COPD), the neuromuscular response to an acute increase in airflow produced by external flow resistive loads (FRL) is impaired. The present study compared the response to FRL of 15 subjects with airway obstruction due to asthma and that of 15 normal subjects. FRL were applied during progressive hypercapnia and isocapnic hypoxia produced by rebreathing techniques to permit the response to be assessed at the same degree of CO2 or O2 drive. The neuromuscular response to FRL was assessed from the airway occlusion pressure developed 100 msec after the onset of inspiration (P100), as well as ventilation. During control rebreathing, ventilatory responses to hypercapnia (ratio of change in minute ventilation to change in PCO2, delta VE/delta PCO2) and hypoxia (ratio of change in VE to the change in percentage of O2 saturation, delta VE/deltaSO2) were the same in asthmatic and normal subjects despite differences in the mechanics of breathing. The P100 response to hypercapnia delta P100/delta PCO2) and hypoxia (delta P100/delta SO2) as well as absolute P100 at any given degree of O2 and CO2 drive was greater during control rebreathing in asthmatics than in normal subjects (P less than 0.05). FRL values of 9 and 18 cm H2O per L per sec applied during either hypercapnia or hypoxia increased the occlusion pressure to a greater extent in asthmatics than in normal subjects. Methacholine-induced bronchoconstriction was used to test the effect of acute airway obstruction on the response to FRL. Bronchoconstriction was associated with an increase in the P100 response to hypercapnia and to FRL, despite increases in lung volume and decreases in inspiratory muscle force. We conclude that: (1) asthmatics with airway dysfunction have an increased nonchemical drive to breathe mediated at least in part by sensory receptors in the airways; (2) asthmatics with airway obstruction respond supernormally to acute changes in resistance to airflow, unlike subjects with COPD. The failure of COPD subjects with prolonged airway obstruction to respond to FRL may be due to adaptation of the sensory mechanisms that respond to changes in airway resistance.
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PMID:The respiratory neuromuscular response to hypoxia, hypercapnia, and obstruction to airflow in asthma. 48 28

20 patients suffering from chronic obstructive lung disease (COLD) were submitted to a 6-month rehabilitation program including breathing exercises only (A) or coupled with bicycle training (B). Functional results obtained at rest were the following: for A: nonsignificant changes in FRC, RV, FEV1, Raw, Pa O2, pH, Pp, VO2 max SL but significant changes (p less than 0.05)for TLC (+ 214 cm3), VC (+ 171 cm3), DL CO (+ 1.79 ml), Pa CO2 (-2.9 mm Hg). For B: similar changes as for A with additional significant changes in PaO2 (+ 7.4 mm Hg) VO2 max SL (+ 250 ml) and Pp (-4 mm Hg). These results, although minimal, are attributed to improved respiratory muscle strength and improved alveolar ventilation. Exercise training adds an increased ability to sustain higher loads.
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PMID:Functional evaluation of a physical rehabilitation program including breathing exercises and bicycle training in chronic obstructive lung disease. 51 31

There is not unanimous agreement in the literature regarding the effects of bleeding on pulmonary gas exchange in polycythemic patients. Spirometry, alveolar arterial O2 and CO2 tension differences, PaO2 breathing 100% oxygen and carbon monoxide-diffusing capacity were measured before and after 1 week of chronic phlebotomy in 4 chronic mountain polycythemic patients. Studies were carried out at 3,700 m above sea level (PB = 491 mm Hg). Before phlebotomy, 2 patients showed abnormal spirometry and gas exchange. Only 1 patient had high PaCO2 and all of them showed low values of PaO2 breathing oxygen. Phlebotomy improved both spirometry and gas exchange. Improvement in arterial oxygen saturation and PaO2 could not be attributed to changes in alveolar ventilation, but rather to better distribution of VA/Qc ratios since physiological dead space decreased. Our results are similar to those reported in polycythemia vera patients. A significant correlation between the changes in PaO2 with phlebotomy and the control PaO2 have been found from 45 polycythemic patients with chronic obstructive pulmonary disease collected from the literature. It is concluded that excessive polycythemia worsened hypoxemia and that phlebotomy improved gas exchange.
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PMID:Phlebotomy improves pulmonary gas exchange in chronic mountain polycythemia. 53 38

Nowadays, domiciliary long-term O2 therapy is given to certain patients with chronic arterial hypoxemia (PaO2 less than 55 mm Hg). However, it is important to exclude cases with severe CO2 retention (PaCO2 greater than 55 mm Hg). Hypoxemic and only slightly hypercapnic patients chiefly suffer from COLD and sometimes from a severe restrictive ventilatory disorder such as chronic bilateral pleural effusions or advanced kyphoscoliosis. The most important precondition for long-term O2 therapy is correct adjustment of all other procedures of pulmonary treatment, as well as total abstention from smoking. Common sources for domiciliary O2 therapy are bottles delivered to the patient's home weekly by the O2-producing firm. A new machine which appears to offer for greater facilities is the O2 concentrator of Rimer-Birlec (Cardiff, Wales). 2 liters O2/min are given via a naso-pharyngeal tube for 15 h per day. Without O2 during 9 h per day, the patient is able to follow appropriate employment. In domiciliary long-term O2 therapy the cost of O2 supply by the O2 concentrator is half that of bottles delivered to the home weekly. The new O2 concentrator for domiciliary long-term O2 therapy is recommended as by far the most economical source of O2. Other sources of O2 such as liquid O2 or chemically produced O2 are uneconomical for domiciliary use. Only hospitals will benefit from supplying their pipelines from a container with liquid oxygen instead of using gaseous O2 from bottles. The cost of the former is 3/4 that of the latter.
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PMID:[Indications and costs of long-term oxygen therapy]. 62 39

Respiratory drive (deltaP 0.1/deltaPCO2) and ventilatory response (deltaVE/deltaPCO2) to CO2 has been estimated in 20 normal subjects and 28 patients with chronic obstructive pulmonary disease (COPD). In patients with COPD, drive and ventilatory response to CO2 were diminished, but no statistical correlation with FEV1, MBC, TLC, FRC, RV/TLC was found. A statistically negative correlation was found between blood bicarbonate and drive or ventilatory response to CO2. Patients with emphysema and normal PaCO2 demonstrated normal deltaP 0.1/deltaPCO2. In contrast, patients with chronic bronchitis with the same pulmonary function abnormalities and hypercapnia had significant diminution of the deltaP 0.1/deltaPCO2. Therefore, we feel that pulmonary function abnormalities alone cannot explain the deltaP 0.1/deltaPCO2 decrease; in most cases there sould coexist a diminished respiratory sensitivity.
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PMID:Respiratory drive in patients with chronic obstructive pulmonary disease. 67 65


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