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• W2185220949 startingPage "L883" @default.
• W2185220949 abstract "Nitric oxide (NO) can be measured in the expired gas of humans and animals, but the source of expired NO (F E NO) and the functional contribution of the various known isoforms of NO synthase (NOS) to the NO measured in the expired air is not known. F E NO was measured in the expired air of mice during mechanical ventilation via a tracheal cannula. F E NO was significantly higher in wild-type B6SV129J +/+ mice than in mice with a targeted deletion of type I (neural) NOS (nNOS, −/−) (6.3 ± 0.9 vs. 3.9 ± 0.4 parts/billion, P = 0.0345, for +/+ and −/− mice, respectively), indicating that ∼40% of the NO in expired air in B6SV129 mice is derived from nNOS. Airway responsiveness to methacholine (MCh), assessed by the log of the effective dose of MCh for a doubling of pulmonary resistance from baseline (ED 200 R L ), was significantly lower in the −/− nNOS mice than in the wild-type mice (logED 200 R L , 2.24 ± 0.07 vs. 2.51 ± 0.06 μg/kg, respectively; P = 0.003). These findings indicate that nNOS significantly contributes to baseline F E NO and promotes airway hyperresponsiveness in the mouse." @default.
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• W2185220949 date "1997-10-01" @default.
• W2185220949 modified "2023-10-14" @default.
• W2185220949 title "Contribution of type I NOS to expired gas NO and bronchial responsiveness in mice" @default.
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• W2185220949 doi "https://doi.org/10.1152/ajplung.1997.273.4.l883" @default.
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