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Nitric oxide and pulmonary circulation.
Med. Sci. Monitor 2002: 8 (8) s.RA178-RA182, bibliogr. 54 poz.
Hasła klasyfikacyjne GBL:
The aim of this review is to outline the characteristics of pulmonary circulation in health and disease and to define the value of exhaled NO (eNO) as a means to assess the involvement of pulmonary cirulation in pathology. The discovery of the endocrine role of the endothelium has generated great interest in its potential role in regulating the vascular tone of the pulmonary vascular bed. Nitric oxide (NO)-mediated, endothelium-dependent relaxation has been demonstrated in the pulmonary arteries of animals and humans. Changes in the NO pathway in pulmonary hypertension are not completely understood. It is clear that NO has an important role in modulating the response to acute hypoxia, increased flow, and shear stress. The amount of exhaled NO (eNO) in different species may be easily measured, reflecting the overall NO metabolism from the lung (thus including epithelial, endothelial and other cell activity). The development of pulmonary hypertension secondary to systemic (systemic sclerosis, chronic heart failure) or pulmonary (COPD) diseases appears to be associated with a decrease in NO production both at rest and during exercise. Chronic inhalation of NO appears to protect against pulmonary hypertension in animal models. Exhaled no is attracting interest for its in vivo ability to represent the features of pulmonary circulation in pathology.
Predictors of change in exercise capacity after comprehensive COPD inpatient rehabilitation.
Med. Sci. Monitor 2002: 8 (11) s.CR740-CR745, tab., bibliogr. 29 poz.
Hasła klasyfikacyjne GBL:
dorośli 45-64 r.ż.
dorośli = 65 r.ż.
Background: In order to evaluate the factors associated with change in exercise capacity after comprehensive inpatient Pulmonary Rehabilitation (IPR) we studied 132 consecutive adults with Chronic Obstructive Pulmonary Disease (COPD) recovering from an acute exacerbation. Material/Methods: Lung function, arterial blood gases, and respiratory muscle strength were measured at baseline. Perceived breathlessness (B), 6-minute walk distance (6MWD) dyspnea at rest and postexertion (D), hospital anxiety and depression (HAD), and health-related quality of life were assessed before (T0) and after (T1) IPR. The patients were divided into two groups depending on the change in 6MWD: Improvers (IM at least +54 meters after IPR, n = 81) or Non-Improvers (NIM less htan 54 meters or no change, n = 51). Results: At T1 61 p.c. of the patients showed improvement as here defined. The IM group showed lower 6MWD and higher B and resting-D at T0than NIM (p 0.05). A stepwise multiple regression analysis was performed using 6MWD change as the dependent variable and anthropometric and physiological measures at T0 as the independent variables. This regression model explained 26 p.c. of the 6MWD-change; 6MWD and PaO2 significantly contributed to this model. Conclusions: In COPD patients recovering from an acute exacerbation, the predicted change in exercise capacity using anthropometric, demographic, clinical, and physiological variables after 2 weeks of comprehensive IPR is likely to be low. The baseline level of exercise performance and arterial oxygenation who the most consistent correlation with change in walking ability in these patients.
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