[Cytochemical criteria of the effectiveness of some methods of resuscitation and treatment in infants born with asphyxia].
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The localization of Mg-stimulated ATPase activity was determined in the sensomotor cortex mitochondria of Wag rats after aminazin administration (15 mg/kg). Apart from normal mitochondria containing no reaction product, a number of altered mitochondria with different localization in them of the ATPase reaction product were recorded. The intact animals showed no sediment in the mitochondria. It is suggested that aminazin-induced increase in ATP-hydrolase activity is caused by two factors: neuroleptic-induced decrease in glycolytic and oxidative cell activity and increased permeability of mitochondrial membranes.
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Adenylate cyclase activity was demonstrated by means of electron microscopic cytochemistry in rat cortical synaptosomes incubated under various conditions. It was found that vinblastine caused remarkable changes in the reaction product localization: the limiting membrane reaction diminished, but the number of synaptosomes were seen to contain a course granular precipitate filling up almost the whole presynaptic cytoplasm. The regulatory role the microtubules play in the distribution of adenylate cyclase on cellular membrane is discussed.
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