Sherman D M, Dolenko V Kh, Zhiliaev L T, Popov V S, Usanov E I, Tsygura I T
Zh Vopr Neirokhir Im N N Burdenko. 1991 Sep-Oct(5):23-6.
It was established in acute experiments on dogs and rabbits that craniocerebral trauma does not lead to the development of torpid shock. In combination of craniocerebral trauma with severe mechanical injury to the thigh or acute massive extracranial blood loss a typical torpid shock develops with death of the animals in the immediate hours. Infusion therapy relieves shock but fails to prevent the development of brain edema. Intravenous injections of procaine hydrochloride have a positive effect in craniocerebral trauma and shock. It is concluded that craniocerebral trauma does not disturb the mechanisms of shock formation and the process takes a course independently of the process of brain edema development.
在对狗和兔子进行的急性实验中发现，颅脑创伤不会导致迟缓性休克的发生。当颅脑创伤与大腿严重机械损伤或急性大量颅外失血合并时，会出现典型的迟缓性休克，动物会在数小时内死亡。输液疗法可缓解休克，但无法预防脑水肿的发展。静脉注射盐酸普鲁卡因对颅脑创伤和休克有积极作用。得出的结论是，颅脑创伤不会干扰休克形成机制，该过程独立于脑水肿发展过程而进行。
