Structural basis of impairment of the external respiratory function in the post-resuscitation period

External enhancement of free-radical processes followed by considerable tissue accumulation of toxic lipid peroxidation products in an early postresuscitation period is the main pathochemical mechanism which causes lung air-blood barrier disturbance. The basis of animal respiratory insufficiency morphogenesis after clinical death is ventilation failure (dis- and atelectasis), circulation disorder (edema, hemorrhage) being secondary. However, morphological examination of lungs of animals after four-minutes clinical death from an acute blood loss and resuscitation showed that it is the severity of circulation disorders that determines the animals condition in the postresuscitation period.