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Chang, Shih-Wen, Janina Czartolomna, and Norbert F. Voelkel. Role of eicosanoidsin staphylococcal a-toxin-induced in the rat. Am. J. Physiol. 262 (Lung CeZZ.MOL. Physiol. 6): L502-L510, 1992.-We investigated the role of arachidonic acid-derived eicosanoidsin staphylococcal a-toxin (cu-T)-induced. Bolus injection of 200and 500pg cw-T into isolatedperfusedrat lungsresulted in increasedpulmonary perfusion pressurefollowed by lung weight gain. Inhibition of pressure changewith papaverine (low4 M) failed to abolish lung edema. Furthermore, cu-T increased the permeability-surface area product in papaverine-treated lungs and causedmarked endothelial cell injury and interstitial edemaas documentedby electron microscopy.cr-T dosedependently increasedlung tissue thromboxane B, (TxB,) levels and leukotriene C, levels. In lungs given 0, 200, and 500 rugof a-T, TxB, (in pg/g wet lung) values were 16.3 t 2.8 , 25.0 t 3.0, and 54.2 t 6.2; and leukotriene C, values were 4.6 t 1.1, 6.7 t 1.2, and 22.1 t 3.8, respectively. Inhibition of cyclooxygenase enzyme with indomethacin ( lob5 M) or lipoxygenase enzyme with 2(12-hydroxydodeca-5,10-dinyl)-3,5,6-trimethyl-l,4-benzoquinone (AA861, 10m5 attenuated the vasoconstriction and preM) vented lung edemadue to low dose(200 pg) but not high dose (500 pg) Q-T. The protective effect of these inhibitors on lung edemais in part due to decreases a-T-stimulated venoconin striction becausea-T-induced increase in lung microvascular pressure
AJP - Lung Cellular and Molecular Physiology – The American Physiological Society
Published: Apr 1, 1992
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