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

Patients with severe COPD may be in a state of ventilatory muscle (VM) fatigue. In these patients, rapid and shallow breathing has been hypothesized to be a compensatory mechanism that prevents more severe fatigue from taking place. To test these hypotheses, we studied the effects of VM resting in a group of patients with severe COPD. Eleven clinically stable patients with COPD and chronic hypercapnia were studied. Six of them (group A) had a seven-day period of negative pressure-assisted ventilation (NPV), and five (group B) with similar functional characteristics served as a control group. Compared with a normal age-matched control group, both A and B groups exhibited significantly lower tidal volume (VT), inspiratory time (TI), total time of the respiratory cycle (Ttot) and Ti/Ttot ratio, decrease in muscle strength, and greater electromyographic activity of diaphragm (EMGd) and parasternal muscles, but similar ventilation and VT/TI. After the study period, group A exhibited significant increase in VT, Ti, and TI/Ttot (p less than 0.05), and decrease in PaCO2 (p less than 0.05), EMGd, and EMGint (p less than 0.05 for both), and a slight but significant increase in maximal inspiratory pressure (MIP) (p less than 0.05). These data suggest that NPV rests VM, increases their strength, and reduces hypercapnia in patients with severe COPD.
 ...
PMID:Changes in ventilatory muscle function with negative pressure ventilation in patients with severe COPD. 229 58

The objective of this study was to compare the response of respiratory drive to progressive hypoxia under eucapnic and hypercapnic conditions in patients with severe COPD. Twenty-five patients with severe COPD and 13 nonsmoking young men were studied. The pressure in the occluded airway measured 0.1 second after the onset of inspiration was used as an index of respiratory drive. The occlusion pressure was measured at levels of SaO2 between 97 and 85 percent while eucapnic. The PETCO2 was then increased 10 mm Hg and the study repeated. The response of respiratory drive to hypoxia as measured by the slope of the regression line relating occlusion pressure to SaO2 was weak and variable in eucapnic hypoxia, and some subjects had no demonstrable response. When mild respiratory acidosis was created by increasing the PETCO2, the response to hypoxia was much greater and occurred in all subjects studied. Respiratory acidosis resulting from acute elevation of the PaCO2 greatly potentiates the increase in respiratory drive in response to hypoxia in normal subjects and in patients with severe COPD. Increase in occlusion pressure may occur with slight degrees of hypoxia when acute hypercapnia is present. These observations suggest that patients with acute respiratory failure complicating COPD, treated with controlled oxygen administration with only partial correction of hypoxia and continued respiratory acidosis, will have high respiratory drive.
 ...
PMID:Interaction of hypoxia and hypercapnia on respiratory drive in patients with COPD. 234 12

The possible role of ventilatory control in relation to sleep apnea has not yet been clarified. We investigated the relationship between awake ventilatory drives to hypoxia and hypercapnia and sleep-disordered breathing in 21 subjects with sleep apnea syndrome. The awake hypoxic ventilatory drive, which was evaluated by occlusion pressure responses, was inversely correlated with the magnitude of maximal oxygen desaturation during sleep as well as the ratio of duration with more than 4 and 10% oxygen desaturation to total sleep time. On the other hand, the awake hypercapnic ventilatory drive was not correlated with these parameters of sleep desaturation. Apnea index and duration were not correlated with the degree of hypoxic or hypercapnic ventilatory drive, respectively. Our study concluded that sleep desaturation is better correlated with hypoxic ventilatory drive than with hypercapnic ventilatory drive in patients with sleep apnea syndrome. These results are different from the results obtained in the patients with COPD in our previous study.
 ...
PMID:Abnormal breathing during sleep and chemical control of breathing during wakefulness in patients with sleep apnea syndrome. 249 71

In 75 COPD patients with (group I) or without (group II) cor Pulmonale, we measured plasma renin activity (PRA), angiotensin I and II (ATI and ATII), and aldosterone (Ald) by RIA. We found that the levels of PRA, ATI, ATII, Ald in group I are all higher than those in 25 healthy subjects and in group II (P less than 0.05, P less than 0.001), The PRA, ATI, ATII, Ald also increased in patients with respiratory failure, especially accompanied by hypercapnia, and in patients with hyponatrium. In addition, the strong correlation was found between PaO2, PaCO2 and RAAS activation. These findings suggest that the activation of RAAS increased significantly in COPD patients with cor pulmonale or with respiratory failure, and the changes may involve in the pathophysiologic process in COPD patients.
 ...
PMID:[The renin-angiotensin-aldosterone system changes in chronic obstructive pulmonary disease]. 263 30

To assess the role of endogenous opioid peptides in ventilatory control in patients with chronic obstructive lung disease, we measured the ventilatory and mouth occlusion pressure responses to hypercapnia and the compensatory response to an inspiratory resistive load in 11 male patients with COPD before and after intravenous administration of naloxone or placebo on 2 separate days. There were no statistically significant differences between naloxone and placebo administration in any index of ventilatory response to CO2 or resistive loading. When an inspiratory resistive load was added during CO2 rebreathing, minute ventilation at PETCO2 = 50 mm Hg in all 11 patients decreased significantly (p less than 0.05) with placebo and naloxone. In response to the inspiratory resistive load, in eight of the 11 patients mouth occlusion pressure (P0.1) did not increase; these eight subjects were classified as noncompensators. Naloxone did not affect the P0.1 response to inspiratory resistive loading, either in the group as a whole or in the subgroup of eight patients classified as noncompensators. Our study was unable to demonstrate that increased activity of endogenous opioid peptides suppresses the ventilatory response to CO2 or resistive loading in patients with chronic obstructive lung disease.
 ...
PMID:Naloxone does not alter response to hypercapnia or resistive loading in chronic obstructive pulmonary disease. 264 73

Elevated endorphin levels in patients with COPD may act to diminish the sensation of dyspnea. Exogenous opioids decrease exertional dyspnea and increase exercise capacity in COPD patients. The purpose of this study was to determine the effects of endogenous opioids on the exercise capacity and control of breathing in patients with COPD. We hypothesized that naloxone, an opioid antagonist, would block the endogenous endorphins and decrease the exercise capacity of our patients. Six patients (mean age, 58.8 +/- 3.2 years) with COPD (mean FEV1, 1.28 +/- 0.46 L) underwent identical incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following the IV administration of naloxone (0.4 mg/kg) (N) or placebo (P) in a randomized, double-blind fashion. Perceived dyspnea (modified Borg scale), breathing patterns, and expired gas levels were compared at rest and at maximal workload (WL). There was no significant difference after N compared with after P in the WL or the duration of work. At Emax there were no significant differences after N compared with after P in ventilation, the level of dyspnea, P0.1, VO2, or VCO2. The ventilatory response to CO2 production during exercise (delta VE/delta VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after N compared with after P. This study does not support the hypothesis that endogenous opioids play a significant role in dampening dyspnea and facilitating exercise in patients with COPD.
 ...
PMID:Effect of naloxone on maximal exercise performance and control of ventilation in COPD. 267 90

The influence of progressive hypoxia and hypercapnia on respiratory mechanics was evaluated in 26 subjects (six normal subjects, seven asthmatic subjects, seven patients with IPD, and six patients with COPD). During separate rebreathing runs of progressive isocapnic hypoxia and normoxic hypercapnia, breath-to-breath changes in RL and Cdyn were determined. In five of the six normal subjects, seven of the seven asthmatic subjects, and six of the seven subjects with IPD, RL decreased with both progressive hypoxia and hypercapnia without a change in Cdyn. In the patients with COPD, the effects of hypoxia and hypercapnia on RL and Cdyn were variable. Compared to normal subjects, the changes in RL during hypoxia and hypercapnia were not significantly different in the asthmatic subjects and the patients with IPD. These data provide evidence that acute progressive hypoxia and hypercapnia are associated with significant changes in Raw in both normal subjects and patients with chronic pulmonary disease.
 ...
PMID:The effects of acute hypoxia and hypercapnia on pulmonary mechanics in normal subjects and patients with chronic pulmonary disease. 273 97

Thirty-six patients, 24 normocapnic (mean age +/- SD: 60 +/- 10) and 12 hypercapnic (mean age +/- SD: 64 +/- 9) were compared with a control group (10 volunteers, mean age +/- SD: 46 +/- 8) for the following patterns of respiratory drive and respiratory timing: (1) mean inspiratory flow (Vt/Ti); (2) mouth occlusion pressure 100 ms after the onset of inspiration (P 0.1) and minute ventilation (Ve); (3) inspiratory duty cycle Ti/Tt). The data suggest COPD "respiratory patterns" which may be characterized by the following features: (1) increased mean inspiratory flow (Vt/Ti); (2) increased P 0.1 (in absolute values), P 0.1/Ve and P 0.1/Vt/Ti; (3) reduction in inspiratory duty cycle (Ti/Tt). Changes are more evident in inspiratory duty cycle among hypercapnic pts. When respiratory obstruction becomes worse and hypercapnia appears, the Ti/Tt decrease could be explained by a reduction in diaphragm muscle work, that can prevent the failure of diaphragmatic contractility.
 ...
PMID:Breathing pattern assessment in normocapnic and hypercapnic patients in chronic obstructive pulmonary disease. 279 45

Acute effects of calcium channel blocker nifedipine were investigated in patients with chronic obstructive pulmonary disease (COPD. In the present study 10 patients were included in the early phase of COPD and 20 patients in the late phase with chronic respiratory insufficiency characterized with resting hypoxemia, hypercapnia and respiratory acidosis. The patients were examined before and after sublingual application of nifedipine (10 mg) or placebo in single-blind study design. Nifedipine did not alter spirometric parameters (FVC, FEV1, FEV1/FVC), except in the late phase of COPD (FEV1). However, acute nifedipine treatment significantly improved resting arterial blood gases: PaO2 increased in both groups while PaCO2 decreased only in the patients in advanced phase of COPD. Additionally, nifedipine increased DLCOSB in the early phase of COPD. Acute nifedipine was found to have a beneficial effect in COPD patients.
 ...
PMID:[The acute effect of nifedipine in chronic obstructive lung disease]. 279 77

The pathogenesis of edema in COPD patients is poorly understood. In 50 COPD patients without cor pulmonale, we measured water sodium and potassium excretion in 24 hours, concentration of sodium and potassium in plasma as well as PRA, ATII and aldosterone levels. We found that PRA, ATII, and aldosterone levels in COPD patients with edema are much higher than those in patients without edema and sodium and water excretion decreased significantly in edematous COPD patients. Elevation of PRA, ATII, and aldosterone correlated with inability to excrete sodium and water. These data suggest that, in conjunction with hypercapnia-hypoxia-mediated disturbance in renal function, stimulation of RAAS, especially the resulting increase of aldosterone may contribute to edema formation in COPD patients.
 ...
PMID:[Role of the renin-angiotensin-aldosterone system in the pathogenesis of edema formation in chronic obstructive pulmonary disease]. 280 68


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>