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- Dharmage, S. C., et al.
(författare)
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Do childhood respiratory infections continue to influence adult respiratory morbidity?
- 2009
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 33:2, s. 237-244
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to examine the influence of childhood respiratory infections on adult respiratory health. In 1992-1994, the European Community Respiratory Health Survey recruited community based samples of 20-44-yr-old people from 48 centres in 22 countries. Study participants completed questionnaires and underwent lung function testing. On average, 8.9 yrs later, 29 centres re-investigated their samples using similar methods. Mixed effects models comprising an estimate for the random variation between centres were used to evaluate the relevant associations. In total, 9,175 patients participated in both studies, of whom 10.9% reported serious respiratory infections (SRI) before 5 yrs of age and 2.8% reported hospitalisation for lung disease (HLD) before 2 yrs if age. SRI was associated with current wheeze (odds ratio (OR) 1.9, 95% confidence interval (CI) 1.7-2.2), asthma (OR 2.5, 95% CI 2.2-3.1), and lower forced expiratory volume in one second (FEV(1); 89 mL; 95% CI 54-126), forced vital capacity (FVC; 49 mL; 95% CI 8-90) and FEV(1)/FVC ratio (-1.2%; 95% CI -1.8- -0.6). Childhood respiratory infections were also associated with new asthma (OR 1.5, 95% CI 1.03-2.0), new wheeze (OR 1.5, 95% CI 1.0-2.4) and persistent wheeze (OR 2.2, 95% CI 1.4-3.6) but not with a decline in lung function. Similar findings were observed for HDL. These associations were significantly consistent across centres. SRI was associated with lower FEV(1) when excluding ever asthmatics and current wheezers. The impact of early infections was significantly larger in subjects exposed to maternal or active smoking. The impact of childhood respiratory infections on the respiratory system may not only last into adulthood but also influence development and persistence of adult respiratory morbidity.
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| 2. |
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| 3. |
- Gonon, AT, et al.
(författare)
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Nitric oxide mediates protective effect of endothelin receptor antagonism during myocardial ischemia and reperfusion
- 2004
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Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 286:5, s. H1767-H1774
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Tidskriftsartikel (refereegranskat)abstract
- Endothelin (ET) receptor antagonism protects from ischemiareperfusion injury. We hypothesized that the cardioprotective effect is related to nitric oxide (NO) bioavailability. Buffer-perfused rat and mouse hearts were subjected to ischemia and reperfusion. At the onset of ischemia, the rat hearts received vehicle, the dual endothelin type A/type B (ETA/ETB) receptor antagonist bosentan (10 μM), the NO synthase inhibitor NG-monomethyl-l-arginine (l-NMMA; 100 μM), the combination of bosentan and l-NMMA or the combination of bosentan, l-NMMA, and the NO substrate l-arginine (1 mM). Hearts from wild-type and endothelial NO synthase (eNOS)-deficient mice received either vehicle or bosentan. Myocardial performance, endothelial function, NO outflow, and eNOS expression were monitored. Bosentan significantly improved myocardial function during reperfusion in rats and in wild-type mice, but not in eNOS-deficient mice. The functional protection afforded by bosentan was inhibited by l-NMMA, whereas it was restored by l-arginine. Myocardial expression of eNOS (immunoblotting) increased significantly in bosentan-treated rat hearts compared with vehicle hearts. Recovery of NO outflow during reperfusion was enhanced in the bosentan-treated rat heart. The endothelium-dependent vasodilator adenosine diphosphate increased coronary flow by 18 ± 9% at the end of reperfusion in the bosentan group, whereas it reduced coronary flow by 7 ± 5% in the vehicle group ( P < 0.001). The response to the endothelium-independent dilator sodium nitroprusside was not different between the two groups. In conclusion, the dual ETA/ETB receptor antagonist bosentan preserved endothelial and cardiac contractile function during ischemia and reperfusion via a mechanism dependent on endothelial NO production.
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