Effect of nonpeptide NK1 receptor antagonist L-703,606 on the edema formation in rats at early stage after deep partial-thickness skin scalding

Objective To investigate the effect and the relevant potential mechanism of nonpeptide neurokinin 1 (NK1) receptor antagonist L-703,606 in the edema formation after burn injury.MethodL-703,606 treatment was performed in Sprague-Dawley (SD) rats at early stage after deep partial-thickness skin scalding. One hundred and fifty two adult male SD rats were used in the study and randomly divided into sham scald (SS, n=8), scald control (SC, n=48), and L-703,606 treatment (LT, n=48) groups. The rats in SC and LT groups were subjected to 20% total body surface area (TBSA) deep partial-thickness skin scalding. Modified Evans blue extravasation, tracing electron microscopy by lanthanum nitrate and mean water content assay were employed to observe and detect the changes of vascular permeability, ultrastructure and edema formation in adjacent tissue to the wounds and in the jejuna of rats at early stage (72 h) after scald.ResultsThe pathological increase of vascular permeability in the periwound tissue and jejunum of rats in LT group were significantly lower than that in SC group (P<0.01), and recuperated earlier. Meanwhile, the changes of water contents of corresponding tissues in LT group were lighter than those in SC group (P<0.01). The ultrastructural changes of the microvessels in the peri-wound tissue of LT group showed that the junctions between microvascular endothelium cells were more narrow than those of SC group, moreover, and the number of opening and the engorgement and cavitation of the vascular endothelium cells decreased, the areosis and edema in perivascular tissue lightened, and the precipitation of the high eletron density lanthanum tracing agent in the interspace of the tissue decreased significantly in LT group.ConclusionsIt is concluded that nonpeptide NK1-receptor antagonist L-703,606 could lighten the vascular permeability and edema formation in the periwound tissue and jejunum, and accelerate the normalization process of pathological changes in the tissues of rats after scald.