[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.
D000818:Animals; D005609:Free Radicals; D008054:Lipid Peroxides / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D011379:Prognosis; D051381:Rats; D012131:Respiratory Insufficiency / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D012151:Resuscitation / Q000009:adverse effects
D005609:Free Radicals; D008054:Lipid Peroxides
Strukturnye osnovy narusheniĭ funktsii vneshnego dykhaniia v postreanimatsionnom periode.