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Mechanisms of mechanical ventilation...

Van Gammeren, Darin.

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Mechanisms of mechanical ventilation-induced oxidative stress in the diaphragm.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Mechanisms of mechanical ventilation-induced oxidative stress in the diaphragm./
作者:	Van Gammeren, Darin.
面頁冊數:	56 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4571.
Contained By:	Dissertation Abstracts International66-09B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3192483
ISBN:	0542354365

Mechanisms of mechanical ventilation-induced oxidative stress in the diaphragm.
Van Gammeren, Darin.

Mechanisms of mechanical ventilation-induced oxidative stress in the diaphragm. - 56 p.

Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4571.

Thesis (Ph.D.)--University of Florida, 2005.

Mechanical ventilation (MV) is associated with oxidative stress and contractile dysfunction in the diaphragm. The pathways responsible for the production of oxidants in the diaphragm during MV remain unknown. To address this issue, these experiments tested the following hypotheses: (1) NADPH oxidase activity is increased during MV and contributes to the oxidative stress and contractile dysfunction of the diaphragm; and (2) diaphragmatic nitric oxide synthase (NOS) levels are elevated in the diaphragm during MV and contribute to nitration of proteins in the diaphragm. To test these postulates, rats were mechanically ventilated for 18 hours with a subset of animals receiving the NADPH oxidase inhibitor, apocynin (4 mg/kg body weight). Diaphragmatic NADPH oxidase and NOS activities were measured along with protein levels of all three NOS isoforms. Further, 3-nitrotyrosine levels in the diaphragm were measured as an index of protein nitration. Compared to control, MV resulted in diaphragmatic oxidative stress and a significant decrease (-10%) in the maximal specific force of the diaphragm. MV did not increase diaphragmatic NADPH oxidase activity above control. Nonetheless, the administration of apocynin attenuated MV-induced contractile dysfunction. Interestingly, treatment with apocynin did not diminish diaphragmatic NADPH oxidase activity but protected the diaphragm against MV-induced oxidative stress. Moreover, MV did not promote an increase in diaphragmatic protein levels of eNOS, nNOS, or iNOS or NOS activity. Consistent with these findings, MV did not elevate diaphragmatic protein levels of 3-nitrotyrosine in any region of the diaphragm including the insoluble, cytosolic, mitochondrial, and membrane protein fractions. Therefore, we conclude that MV-induced oxidative stress in the diaphragm is not due to increases in NADPH oxidase activity or increased NO production by NOS. Moreover, our results suggest that apocynin attenuates the MV-induced diaphragm contractile dysfunction and oxidative stress via its antioxidant properties, not through the inhibition of NADPH oxidase.

ISBN: 0542354365Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Mechanisms of mechanical ventilation-induced oxidative stress in the diaphragm.
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