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Background: The real contribution of nonexacerbated COPD to mortality has not been studied. The aim of our study was to evaluate the impact of nonexacerbated COPD on mortality in patients requiring mechanical ventilation (MV).Methods: This prospective, observational study included critically ill, ventilated patients without evidence of respiratory infection. Patients with COPD comprised the study group. Clinical and demographics variables were recorded. The main end point was ICU mortality.Results: Of the 235 patients included, 60 (25.5%) intubated patients had COPD. The remaining 175 (74.5%) comprised the control group. Those with COPD were more often medical patients who were older and had a higher number of comorbidities and a higher APACHE (Acute Physiology and Chronic Health Evaluation) II score than intubated patients without COPD (P < .05). The overall ICU mortality was 26.3% (62/235) and significantly higher in patients with nonexacerbated COPD (36.7% vs 22.9%, P < .05), with an attributable mortality to COPD of 13.8%. Incidence of ventilator-associated pneumonia was not significantly different between patients with nonexacerbated COPD (11.9/1,000 MV days) and without COPD (16.0/1,000 MV days; P = .40). In the multivariate analysis, only COPD (hazard ratio [HR], 2.1; 95% CI, 1.10-3.94), shock at ICU admission (HR, 2.0; 95% CI, 1.01-4.01), and medical condition (HR, 1.7; 95% CI, 1.01-3.18) were independently associated with mortality.Conclusions: Intubated patients with nonexacerbated COPD were not exposed to a higher risk of ventilator-associated pneumonia but had a higher rate of mortality. [ABSTRACT FROM AUTHOR]

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We hypothesized that resistive breathing of moderate to high intensity might increase diaphragm oxidative stress, which could be partially attenuated by antioxidants. Our objective was to assess the levels of oxidative stress in the dog diaphragm after respiratory muscle training of a wide range of intensities and whether N-acetyl-cysteine (NAC) might act as an antioxidant. Twelve Beagle dogs were anesthetized with 1% propophol, tracheostomized, and subjected to continuous inspiratory resistive breathing (IRB) (2 h/day for 2 wk). They were further divided into two groups (n = 6): NAC group (oral NAC administration/24 h for 14 days) and control group (placebo). Diaphragm biopsies were obtained before (baseline biopsy) and after (contralateral hemidiaphragm) IRB and NAC vs. placebo treatment. Oxidative stress was evaluated in all diaphragm biopsies through determination of 3-nitrotyrosine immunoreactivity, protein carbonylation, hydroxynoneal protein adducts, Mn-SOD, and catalase, using immunoblotting and immunohistochemistry. Both protein tyrosine nitration and protein carbonylation were directly related to the amount of the respiratory loads, and NAC treatment abrogated this proportional rise in these two indexes of oxidative stress in response to increasing inspiratory loads. A post hoc analysis revealed that only the diaphragms of dogs subjected to high-intensity loads showed a significant increase in both protein tyrosine nitration and carbonylation, which were also significantly reduced by NAC treatment. These results suggest that high-intensity respiratory loading-induced oxidative stress may be neutralized by NAC treatment during IRB in the canine diaphragm. [ABSTRACT FROM AUTHOR]

Rationale: Oxidative stress is involved in the skeletal muscle dysfunction observed in patients with severe chronic obstructive pulmonary disease (COPD). We hypothesized that the diaphragms of such patients might generate greater levels of oxidants than those neutralized by antioxidants. Objectives: To assess the levels of both oxidative and nitrosative stress and different antioxidants in the diaphragms of those patients, and to analyze potential relationships with lung and respiratory muscle dysfunctions. Methods and Measurements: We conducted a case-control study in which reactive carbonyl groups, hydroxynonenal-protein adducts, antioxidant enzyme levels, nitric oxide synthases, and 3-nitrotyrosine formation were detected using immunoblotting and immunhistochemistry in diaphragm specimens (thoracotomy) obtained from six patients with severe COPD, six patients with moderate COPD, and seven control subjects. Main Results: Diaphragms of patients with severe COPD showed both higher protein carbonyl groups and hydroxynonenal-protein adducts than control subjects. When only considering patients with COPD, negative correlations were found between carbonyl groups and airway obstruction, and between hydroxynonenal-protein adducts and respiratory muscle strength. Although diaphragmatic neuronal nitric oxide synthase did not differ among the three groups and no inducible nitric oxide synthase was detected in any muscle, muscle endothelial nitric oxide synthase was lower in patients with severe COPD than in control subjects. Muscle nitrotyrosine levels were similar in both patients with severe COPD and control subjects. Conclusions: This study shows that oxidative stress rather than nitric oxide is likely to be involved in the respiratory muscle dysfunction in severe COPD. [ABSTRACT FROM AUTHOR]