[Hypoxia of the central nervous system in rats during acceleration brain injury].

The authors present the results of investigations of the effects of acceleration craniocerebral injury in rats on PaO2 and resulting central nervous system hypoxia. PaO2 fall by 30% of the control value occurred in 25% of rats and in the group of most severe injury this fall amounted to 36% already 1 minute after injury. After 4 minutes this fall rose to 70%. In all animals with injury-induced hypoxia autopsy examination demonstrated on gross inspection acute pulmonary oedema: the weight of the lungs and the lung-body weight index were nearly twice as high as in the animals without oedema. The authors discuss the possible pathological mechanisms of acute neurogenic lung oedema and reach the conclusion that it may be due to excessive, pathological discharge of the sympathetic nervous system. Since the intracranial part of the vascular bed in rats reacts to acceleration trauma with acute spasm, it may be that this factor, together with central nervous system hypoxia caused by neurogenic lung oedema may play a significant role in traumatic secondary central nervous system injury. This risk occurs also in humans with severe brain stem trauma.