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Congenital NOS2 deficiency prevents impairment of hypoxic pulmonary vasoconstriction in murine ventilator-induced lung injury
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Titel: |
Congenital NOS2 deficiency prevents impairment of hypoxic pulmonary vasoconstriction in murine ventilator-induced lung injury |
In: | American Journal of Physiology-Lung Cellular and Molecular Physiology, 293, 2007, 5, S. L1300-L1305 |
veröffentlicht: |
American Physiological Society
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Umfang: | L1300-L1305 |
ISSN: |
1040-0605 1522-1504 |
DOI: | 10.1152/ajplung.00396.2006 |
Zusammenfassung: | <jats:p> Hypoxic pulmonary vasoconstriction (HPV) preserves systemic arterial oxygenation during lung injury by diverting blood flow away from poorly ventilated lung regions. Ventilator-induced lung injury (VILI) is characterized by pulmonary inflammation, lung edema, and impaired HPV leading to systemic hypoxemia. Studying mice congenitally deficient in inducible nitric oxide synthase (NOS2) and wild-type mice treated with a selective NOS2 inhibitor, l- N<jats:sup>6</jats:sup>-(1-iminoethyl)lysine (l-NIL), we investigated the contribution of NOS2 to the impairment of HPV in anesthetized mice subjected to 6 h of either high tidal volume (HV<jats:sub>T</jats:sub>) or low tidal volume (LV<jats:sub>T</jats:sub>) ventilation. HPV was estimated by measuring the changes of left lung pulmonary vascular resistance (LPVR) in response to left mainstem bronchus occlusion (LMBO). LMBO increased the LPVR similarly in wild-type, NOS2<jats:sup>−/−</jats:sup>, and wild-type mice treated with l-NIL 30 min before commencing 6 h of LV<jats:sub>T</jats:sub> ventilation (96% ± 30%, 103% ± 33%, and 80% ± 16%, respectively, means ± SD). HPV was impaired in wild-type mice subjected to 6 h of HV<jats:sub>T</jats:sub> ventilation (23% ± 16%). In contrast, HPV was preserved after 6 h of HV<jats:sub>T</jats:sub> ventilation in NOS2<jats:sup>−/−</jats:sup> and wild-type mice treated with l-NIL either 30 min before or 6 h after commencing HV<jats:sub>T</jats:sub> ventilation (66% ± 22%, 82% ± 29%, and 85% ± 16%, respectively). After 6 h of HV<jats:sub>T</jats:sub> ventilation and LMBO, systemic arterial oxygen tension was higher in NOS2<jats:sup>−/−</jats:sup> than in wild-type mice (192 ± 11 vs. 171 ± 17 mmHg; P < 0.05). We conclude that either congenital NOS2 deficiency or selective inhibition of NOS2 protects mice from the impairment of HPV occurring after 6 h of HV<jats:sub>T</jats:sub> ventilation. </jats:p> |
Format: | E-Article |
Quelle: | American Physiological Society (CrossRef) |
Sprache: | Englisch |