دورية
Platelet-Activating Factor and Bacteremia-Induced Pulmonary Hypertension
| العنوان: | Platelet-Activating Factor and Bacteremia-Induced Pulmonary Hypertension |
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| المؤلفون: | Clavijo, Leonardo C, Carter, Mary B, Matheson, Paul J, Wills-Frank, Lisa A, Wilson, Mark A, Wead, William B, Garrison, R.Neal |
| المصدر: | Journal of Surgical Research; February 2000, Vol. 88 Issue: 2 p173-180, 8p |
| مستخلص: | Background.Acute lung injury is a common complication of gram-negative sepsis. Pulmonary hypertension and increased lung vascular permeability are central features of lung injury following experimental bacteremia. Platelet-activating factor is a prominent proinflammatory mediator during bacterial sepsis. Our previous studies have demonstrated that exogenous administration of platelet-activating factor (PAF) induces pulmonary edema without causing pulmonary hypertension. Interestingly, inhibition of PAF activity during Escherichia colibacteremia prevents the development of both pulmonary hypertension and pulmonary edema. These data suggest that PAF contributes to pulmonary hypertension during sepsis, but that this is unlikely to be a direct vascular effect of PAF. The goal of the present study was to investigate the mechanism by which acute E. colibacteremia induces pulmonary injury and to define the role that PAF plays in this injury. We hypothesized that the effects of PAF on pulmonary hypertension during bacteremia are due to the effects of PAF on other vascular mediators. Several studies suggest that PAF induces the expression of endothelin-1 (ET), a potent peptide vasoconstrictor. Further, our previous studies have implicated ET as a central mediator of systemic vasoconstriction during bacteremia. We therefore sought to assess whether ET is modulated by PAF. E. colihas also been demonstrated to increase endothelial production of nitric oxide (NO), which contributes to maintenance of basal vascular tone in the pulmonary circulation. We hypothesized that PAF might increase pulmonary vascular resistance during bacteremia by activating neutrophils, increasing expression of ET, and decreasing the tonic release of NO. Furthermore, we hypothesized that hypoxic vasoconstriction did not contribute to pulmonary vasoconstriction during the first 120 min of E. colibacteremia. |
| قاعدة البيانات: | Supplemental Index |
Full Text Finder | تدمد: | 00224804 10958673 |
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| DOI: | 10.1006/jsre.1999.5748 |