[Experimental studies on the pathogenesis of adult respiratory distress syndrome using 111In-labeled polymorphonuclear leukocytes].

This study was undertaken to clarify the mechanism of the development of ARDS and to improve its treatment by studying the role of polymorphonuclear leukocytes (PMNs) in an endotoxin shock model of rats. PMNs from a rat were labeled with 111In by the use of tropolone and were injected into rats pretreated with endotoxin. Then the biodistribution of PMNs was studied by either counting the radioactivity of excised organs or using a gamma scintillation camera on the anesthetized rats. The two methods facilitated to observe the distribution of PMNs fairly a short time after the injection of endotoxin. There was a significantly higher radioactivity in the lungs of the endotoxin group than in the control group. The accumulation of PMNs into the lungs occurred immediately after endotoxin injection. In rats depleted of the complement by cobra venom factor (CVF), an increase in radioactivity in the lung was not observed. These results indicate that the complement system is involved in the pathogenesis of ARDS. When rats were injected with methylprednisolone, the pulmonary accumulation of 111In-PMNs by endotoxin were suppressed. This is an experimental support of possible beneficial effects of corticosteroids in the treatment of ARDS.