| The role of pulmonary capillary pressure in the oxygen free radical- induced acute lung injury. |
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Chul Gyu Yoo1, Young Whan Kim2, Sung Koo Han2, Young Soo Shim2, Keun Youl Kim2, Yong Chol Han2 |
1Department of Internal Medicine, Kangnam General Hospital Public Corporation, Seoul, Korea
2Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea |
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| Abstract |
Background
Regardless of its causes, acute lung injury is characterized pathophysiologically by increased pulmonary arterial pressure and the protein.rich edema. Many inflammatory mediators are known to be involved in the pathogenesis of acute lung injury, including oxygen free radicals (OFR).
But the changes in pulmonary capillary pressure in the OFR-induced acute lung injury is not clear.
While the pulmonary edema characterized by the movement of fluid and solutes is dependent on the pressure gradient and the alveolar-capillary permeability, the role of pulmonary capillary pressure in the development of pulmonary edema is also not well understood.
Methods
Male Sprague-Dawley rats were divided into 5 groups: normal control (n=5) , xanthine / xanthine oxidase (X / XO)-treated group (n=7) , catalase.pretreated group (n=5), papaverine pretreated group (n=7) , and indomethacin-pretreated group (n= 5). In isolated perfused rat lungs, the sequential changes in pulmonary arterial pressure, pulmonary capillary pressure by double occlusion method, and lung weight as a parameter of pulmonary edema were determined.
Results
Pulmonary arterial pressure and pulmonary capillary pressure were increased by X / XO. This increase was significantly attenuated by catalase and papaverine, but indomethacin did not prevent the X / XO.induced increase. Lung weight gain was also observed by X / XO perfusion. It was prevented by catalase. Papaverine did not completely block the increase, but significantly delayed the onset. Indomethacin had no effect on the increase in lung weight.
Conclusions
These data suggest that increased pulmonary capillary pressure by OFR may aggravate pulmonary edema in the presence of increased alveolar-capillary permeability and this may not be mediated by cyclooxygenase metabolites |
| Key Words:
Oxygen free radicals, Pulmonary capillary pressure, Acute lung injury |
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