Introduction:

Acute respiratory distress syndrome (ARDS) in the endothelium causes vasoconstriction, adhesion of inflammatory cells and development of pulmonary edema, pulmonary hypertension and thrombosis. This endothelial damage lowers the production of nitric oxide (NO) and increases the expression of endothelin-1 (ET-1). The aim of this study was to evaluate the effect of pretreatment with L-arginine in OA-induced ALI.

Material and methods:

Hemodynamic, gasometric, microscopic, immunohistochemical and plasma concentration of ET-1 and ET-1 y ETB were analyzed in an experimental model of AO-induced ARDS. The dogs were divided into three study groups: I (n = 6), control; II (n = 6), OA-induced ARDS at an IV dose of 0.09 mL/kg, untreated, and III (n = 6), pretreatment with L-arginine at 0.125 g/min/IV in 250 mL of 0.09% saline and OA-induced ARDS.

Results:

The hemodynamic, blood gas and gravimetric findings revealed that groups II and III developed ARDS. Intrapulmonary shunt increased in groups II and III (p < 0.05, ANDEVA Dunnett). PaO2/FiO2 decreased in groups II and III with a significant difference with group I (p < 0.05, ANDEVA MR Dunnett). The group III showed less inflammatory infiltrate and edema in lung tissue. Plasma levels of ET-1 showed a higher value for group III. The in situ expression of ET-1 and ETB was higher for group II than for group III.

Conclusions:

Pretreatment with L-arginine in an experimental model of AO-induced acute SIRA attenuated hypoxic pulmonary vasoconstriction (HPV) leading to deterioration in intrapulmonary shunting. However, the edema and inflammatory infiltrate in the tissue decreased, therefore, in this model you can only consider a potential attenuating effect on lung inflammation during the acute phase by L-arginine.