Phospholipasic and prophospholipasic activities in bronchoalveolar lavage fluid in severe acute pulmonary disease with or without ARDS

Abstract

Bronchoalveolar lavages were performed in 21 patients undergoing mechanical ventilation: Group I: coma due to sedative overdose (11 cases), without pulmonary impairment, serving as control group; Group II: severe acute pulmonary disease without ARDS (5 cases); Group III: patients with ARDS (5 cases). In the recovered fluid we measured: total proteins (P) and phospholipids (PL), phospholipasic (PLase) and prophospholipasic (PPLase) activities. In ARDS group, considerable increase of P, (p less than 0.001), and a doubling of PL (p less than 0.02) was found. Total PLase activity was present in all three groups, with a higher mean level in Group III (p less than 0.01). PPLase activities were low or undetectable in four patients of this group. PLase/PL ratio was increased in acute respiratory insufficiency, with or without ARDS, suggesting an increase of surfactant catabolism. The decrease of this ratio when pulmonary function improved, or its increase after deterioration suggest that it is related to changes of surfactant.

Down-regulation by prostaglandins of type-II phospholipase A2 expression in guinea-pig alveolar macrophages: a possible involvement of cAMP

“…In patients with adult respiratory distress syndrome, a positive correlation has been demonstrated between PLA # -II levels measured in the bronchoalveolar lavage fluid and the severity of the disease [10,11]. Intratracheal injection of lipopolysaccharide (LPS) into blood-free isolated rat lungs stimulated PLA # -II mRNA expression, suggesting that resident pulmonary cells such as alveolar macrophages (AM) may account for PLA # -II production [12].…”

Inhibition of LPS‐induced chemokine production in human lung endothelial cells by lipid conjugates anchored to the membrane

“…sPLA 2 has been assumed to play an important role in the development of ARDS, as elevated PLA 2 activity in the serum of patients with septic shock was found to be associated with an increased risk for the development of ARDS (Vadas & Pruzanski, 1993), and increased sPLA 2 levels in bronchoalveolar‐fluid correlated with the severity of ARDS (Offenstadt et al ., 1981). This was supported by the finding that sPLA 2 infusions into the pulmonary circuit of dogs and rats (Littner & Lott, 1990) induce changes resembling those observed in ARDS, and intratracheal administration of sPLA 2 caused similar histological injury and clinical symptoms (Edelson et al ., 1991).…”

Metabolism of Pulmonary Surfactant

“…Breakdown in the alveolar space from the action of alveolar enzymatic activity also does not appear to be a major pathway in the normal lung except perhaps in the rat, 82 ' 83 but alveolar enzymatic activity may be an important consideration in conditions in which phospholipase release into the alveolar space occurs, as can happen during lung injury. 84 ' 85…”