Prostaglandin F_2α Metabolite Levels in Arterial Blood, Right Lymph Duct Lymph and Respiratory tract Fluid in Alloxan-induced Pulmonary Edema.

Abstract

Alloxan-induced pulmonary edema was produced in dogs in order to investigate the pathogenesis of pulmonary edema and prostaglandin release in lung. Pulmonary edema was induced in dogs by intravenous injection of alloxan (150mg/kg), and samples from arterial blood, right lymph duct (RLD) lymph and respiratory tract fluid were assayed for the measurement of the main metabolite, 15-keto 13, 14 dihydro PGF_2α. Arterial plasma concentrations of the PGF_2α-M were 0.75±0.17 (SEM) in controls, and increased to 2.96±0.90ng/ml (p<0.005), when pulmonary edema was induced. PGF_2α-M levels in RLD lymph increased from 1.19±0.43 to 3.38±0.95ng/ml after onset of edema (p<0.0125). Respiratory tract fluid during the presence of edema contained about the same level of PGF_2α-M with that in RLD lymph. Appearing edema, RLD lymph flow increased from 3.3 to 17.8ml/h, and lymph/plasma protein ratio increased from 0.56 to 0.86. Electron microscopy examination showed swelling of the alveolar interstitium, desquamation of the type I epithelium and an increase in number of pinocytotic vesicles and vacuoles in the capillary endothelium. These high concentrations of PGF_2α-M in arterial blood, RLD lymph, and respiratory tract fluid suggested an enhanced release of PGF_2α or its precursor in the lung along with the induction of pulmonary edema. The findings by electron microscopy indicated the damage of the type I epithelium as well as capillary endothelium in alloxaninduced pulmonary edema.