There have been many studies of the causes of pulmonary edema. However, there are few studies of the factors which affect the further accumulation of fluid in lungs which are already edematous. This is an important area of investigation because the continued accumulation of more edema fluid may affect the severity and duration of the pulmonary complications in critically ill patients. This proposal is designed to investigate the factors involved in fluid exchange in edematous lungs. The preparation to be used allows for the collection of lymph from continously weighed lungs. With this preparation, the rate of edema formation can be determined from the rate of lung weight gain and changes in the microvascular filtration rate may be assessed from the weight gain and lymph flow rates. Edema will be produced by elevated microvascular pressure. As edema formation progresses, the microvascular membrane reflection coefficient to protein and the membrane filtration coefficient, will be determined. These measurements should indicate if there is any change in microvascular permeability. Measurement of lymph flow should indicate if there is any decrease in lymphatic function during edema. Furthermore, estimates of 1) the pressure driving lymph from the lungs and 2) the effective lymph vessel resistance should yield valuable information about the cause of changes in lymph flow as edema develops. Information obtained from the permeability and lymph flow studies will be correlated with histologic determination of the site of edema fluid accumulation within the lung (interstitial vs intraalveolar). This study should allow for the evaluation of the factors involved in the rate at which fluid moves into the lung tissue through the microvascular membrane and the factors which are involved in fluid removal via the lymphatic vessels.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Research Project (R01)
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Respiratory and Applied Physiology Study Section (RAP)
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University of Texas Health Science Center Houston
Schools of Medicine
United States
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Gabel, J C; Dhother, S; Drake, R E (1994) Increased lymphatic pressure without increased neck vein pressure during intravenous infusions. Am J Physiol 266:R1596-8
Garewal, D; Gallagher, H; Drake, R E et al. (1993) Washout of protein in dog lung lymph. J Appl Physiol 75:1168-70
Drake, R E; Anwar, Z; Kee, S et al. (1993) Intestinal lymphatic pressure increases during intravenous infusions in awake sheep. Am J Physiol 265:R703-5
Gallagher, H; Garewal, D; Drake, R E et al. (1993) Estimation of lymph flow by relating lymphatic pump function to passive flow curves. Lymphology 26:56-60
Drake, R E; Gabel, J C (1992) Diaphragmatic lymph vessel drainage of the peritoneal cavity. Blood Purif 10:132-5
Gabel, J C; Drake, R E (1992) Increased venous pressure causes increased thoracic duct pressure in awake sheep. J Appl Physiol 73:654-6
Drake, R E; Abbott, R D (1992) Effect of increased neck vein pressure on intestinal lymphatic pressure in awake sheep. Am J Physiol 262:R892-4
Allen, S J; Fraser, R E; Laurent, U B et al. (1992) Turnover of hyaluronan in the rabbit pleural space. J Appl Physiol 73:1457-60
Drake, R E; Gabel, J C (1991) Effect of outflow pressure on intestinal lymph flow in unanesthetized sheep. Am J Physiol 260:R668-71
Drake, R E; Gabel, J C (1991) Estimation of the pulmonary microvascular reflection coefficient to protein in dogs. J Appl Physiol 71:94-8

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