New insight concerning transvascular formation and reabsorption of pulmonary edema has been provided by novel stop-flow procedures developed in our laboratory. These studies indicate that elevations in pulmonary vascular pressures result in leakage primarily from the venous side of the pulmonary exchange vessels but not rom the arterial side. They have also shown that when perfusion is briefly interrupted, excess interstitial fluid can be forced back into the vasculature of isolated rat lungs by simultaneously raising airspace and pleural pressures. Reabsorption of fluid under these circumstances can occur even in the presence of very low protein concentrations in the perfusate. This observation indicates that strictly hydrostatic pressure gradients can effect reabsorption of edema from the pulmonary interstitium, a phenomenon which has not been documented in other organs. However no fluid reabsorption occurs unless the lungs are inflated, suggesting that fluid returns to extraseptal vessels which ar e kept open when the lungs are inflated. We hypothesize that the unique capacity of the lung to reabsorb edema fluid under these circumstances is based upon the fact that lung inflation prevents compression of extraseptal portions of the venous microvasculature, which are pulled open as the lungs are inflated. This study will utilize the uptake of 201/Tl from the perfusate to calculate the fraction of samples collected from the pulmonary outflow which were within the pulmonary exchange vessels during the stop-flow interval. Experiments will be conducted to compare the sites of edema formation, solute exchange, and fluid reabsorption with hypertonic solutions of small and large molecules. It is anticipated that hypertonic solutions of small molecules will result in cellular dehydration all along microvasculature whereas the sites of fluid reabsorption with protein and other macromolecules will depend upon their molecular size. We will also seek to confirm that NO production is greater in venous at suites which inhibit edema formation and will investigate the effects of NO on transvascular fluid transport. The effects of lung injury caused by high vascular pressures, over distention of the lungs, acid aspiration and infections of the oleic acid will be investigated.
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| Effros, Richard M; Su, Jennifer; Casaburi, Richard et al. (2005) Utility of exhaled breath condensates in chronic obstructive pulmonary disease: a critical review. Curr Opin Pulm Med 11:135-9 |
| Effros, Richard M; Dunning 3rd, Marshall B; Biller, Julie et al. (2004) The promise and perils of exhaled breath condensates. Am J Physiol Lung Cell Mol Physiol 287:L1073-80 |
| Effros, R M; Olson, L; Lin, W et al. (2003) Resistance of the pulmonary epithelium to movement of buffer ions. Am J Physiol Lung Cell Mol Physiol 285:L476-83 |
| Effros, Richard M; Bosbous, Mark; Foss, Bradley et al. (2003) Exhaled breath condensates: a potential novel technique for detecting aspiration. Am J Med 115 Suppl 3A:137S-143S |
| Effros, Richard M; Biller, Julie; Foss, Bradley et al. (2003) A simple method for estimating respiratory solute dilution in exhaled breath condensates. Am J Respir Crit Care Med 168:1500-5 |
| Effros, Richard M; Hoagland, Kelly W; Bosbous, Mark et al. (2002) Dilution of respiratory solutes in exhaled condensates. Am J Respir Crit Care Med 165:663-9 |
| Crandall, Edward D; Effros, Richard M (2002) Historical perspectives on lung edema clearance. J Appl Physiol 93:1527-32 |
| Lin, W; Hogan, G; Effros, R M (2001) Relationship of ultrafiltration and anastomotic flow in isolated rat lungs. Microcirculation 8:321-34 |
