Changes in the polymorphonuclear leukocyte infiltration, hemorrhage and plasma exudation in the pulmonary tissue in rats with smoke inhalation injury / 中华烧伤杂志

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the different velocity of polymorphonuclear neutrophil (PMN) infiltration, erythrocyte diapedesis and plasma exudation into the pulmonary tissue of the rats inflicted with smoke inhalation injury, so as to explore the different mechanisms of their existence in rat pulmonary tissue after inhalation injury.</p><p><b>METHODS</b>The rat smoke inhalation injury model was employed in the study. Wistar rats were inflicted with smoke inhalation injury, and then sacrificed at 1, 3, 6, 12 and 24 post injury hours (PIH). 131I-BSA, 99mTc-PMN or 99mTc-erythrocytes (RBC) were injected into rat pulmonary tissue 1 hour before sacrifice. Isotonic saline was infused into blood vessel to wash out circulation blood. Then the pulmonary tissue samples were harvested for gamma-value counting and then weighed. The infiltration of 131I-BSA, 99mTc-PMN or 99mTc-RBC in pulmonary tissue per gram and per minute was calculated, and MPO content was measured by phosphate T-tolidine method.</p><p><b>RESULTS</b>The amount of RBC diapedesis in rat lung tissue peaked at 1 PIH, decreased thereafter and approached to normal level at 24 PIH. The amount of PMN infiltration increased at 3 PIH, slightly decreased at 6 PIH but still higher than that in normal tissue, and increased again at 24 PIH. The pulmonary tissue content of MPO gradually increased from 1 PIH to 24 PIH. The pulmonary tissue content of 131I-BSA began to increase at 1 PIH and peaked at 6 PIH, and remained higher than that in normal tissue till 24 PIH.</p><p><b>CONCLUSION</b>Even though there was remarkable postburn increase in the erythrocyte diapedesis, neutrophil infiltration and albumin exudation with different peak time points (1, 3 and 6 PIH, respectively), Inflammation seemed not to be the premise of erythrocyte diapedesis, while the secondary inflammatory reaction might be the main cause of pulmonary edema.</p>