The purpose of the proposed studies is to examine the mechanisms that have been postulated to increase the pulmonary vascular permeability to fluid and proteins during activation of the complement system. Studies will be made in sheep in which pulmonary lymph will be collected to assess alterations in pulmonary fluid and protein exchange. These studies will examine the contributions of the putative factors postulated to increase vascular permeability after complement activation induced with cobra venom factor or zymosan activated plasma. The participation of fibrinogen, leukocytes, and platelets will be assessed by depletion studies. The roles of oxygen radicals, and plasmin, will be examined by preventing their formation during complement activation. The postulated roles of TxA2, PGI2, PGE2, and alveolar hypoxia in modulating the degree of lung vascular injury after complement activation will also be examined. These studies will help to elucidate the mechanism of increased vascular permeability after complement activation.
| Johnson, A; Lo, S K; Blumenstock, F B et al. (1987) CVF-induced decomplementation: effect on lung transvascular protein flux after thrombin. J Appl Physiol 62:863-9 |
| Johnson, A; Perlman, M B; Blumenstock, F A et al. (1986) Superoxide dismutase prevents the thrombin-induced increase in lung vascular permeability: role of superoxide in mediating the alterations in lung fluid balance. Circ Res 59:405-15 |
| Johnson, A; Cooper, J A; Malik, A B (1986) Effect of complement activation with cobra venom factor on pulmonary vascular permeability. J Appl Physiol 61:2202-9 |
| Garcia-Szabo, R R; Johnson, A; Malik, A B (1986) Leukocytes are required for the trypsin-induced increase in lung vascular permeability. Am J Pathol 124:377-83 |
| Johnson, A; Malik, A B (1985) Pulmonary transvascular fluid and protein exchange after thrombin-induced microembolism. Differential effects of cyclooxygenase inhibitors. Am Rev Respir Dis 132:70-6 |
