Esrig B C, Fulton R L
Ann Surg. 1975 Sep;182(3):218-27. doi: 10.1097/00000658-197509000-00005.
Dogs were submitted to hermorrhagic shock, resuscitated shock and resuscitated shock plus a pulmonary bacterial insult. Pulmonary familure was absent in dogs submitted only to shock or to shock and its resuscitation. The addition of usually sub-lethal amounts of micro-organisms to the shock-resuscitated lung caused rapid death from pulmonary failure. Pulmonary failure was demonstrated by increased lung weight, hypoxemia, decreased compliance and a hemorrhagic destruction of lung tissue. These findings strongly support recent concepts of an infective genesis of "shock lung" in man.
将狗置于失血性休克、复苏后休克以及复苏后休克加肺部细菌感染的状态。仅经历休克或休克及复苏的狗未出现肺衰竭。在经历休克复苏的肺中加入通常为亚致死量的微生物会导致因肺衰竭迅速死亡。肺衰竭表现为肺重量增加、低氧血症、顺应性降低以及肺组织出血性破坏。这些发现有力地支持了人类“休克肺”感染性发病机制的最新概念。