[Membrane damage in brain subcellular structures in terminal states and in the postresuscitation period].
Animal experiments were made to study and compare enzymatic activity of brain tissue mitochondria and microsomes treated and untreated with Tween-80 and Triton-X-100. In Mongolian gerbils, the 10-minute brain ischemia induced by bilateral carotid occlusion led to the labilization of the membranes of microsomal fractions, which did not return to normal an hour after resuscitation. The destructive effect of ischemia combined with clinical death from mechanical aspnyxia was similar to that of Triton-X-100. The ten-minute clinical death from ventricular fibrillation due to electroshock in dogs labilized lysosomal membranes. During the first hour after resuscitation and especially during the first 24 hours, the treatment of crude mitochondria with Tween-80 did not activate alkaline phosphatase and plasminogenic activator as compared with the control group.
D000818:Animals; D001921:Brain / Q000648:ultrastructure*; D003643:Death; D004285:Dogs; D005260:Female; D005849:Gerbillinae; D007425:Intracellular Membranes / Q000648:ultrastructure; D008297:Male; D008861:Microsomes / Q000648:ultrastructure; D008928:Mitochondria / Q000648:ultrastructure; D012151:Resuscitation
Povrezhdenie membran subkletochnykh struktur golovnogo mozga pri terminal'nykh sostoianiiakh i v postreanimatsionnom periode.