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[Increase in the cAMP content of mouse brain cells in ischemia and inhibition of this effect by certain biologically active compounds].
Anoxia (during 2 minutes after decapitation) produced a significant elevation of cAMP contents (up to 410%) in mouse brain cells. This effect was abolished by an intraperitoneal injection of alloxan (A), morphine (M), and ethanol (E) 30 minutes before decapitation, and after a 2 minutes diethyl ether (DE) inhalation. It was found that anoxia produced some decrease in phosphodiesterase (FDE) activity. A preliminary injection of A and E produced an activation of FDE; M and DE did not change FDE significantly. Mechanisms of action of all the four agents on the cAMP content under anoxia are different. A and E produced a rapid cAMP hydrolysis on stimulating the activity of FDE, M and DE inhibited apparently adenylate cyclase. The activation of adenylate cyclase due to anoxia is considered as one of the initial steps in the cell injury extention.
Brain Chemistry, Male, Mice, Inbred C57BL, Mice, Ethanol, Morphine, Alloxan, Cyclic AMP, Animals, Hypoxia, Brain, Ether
Brain Chemistry, Male, Mice, Inbred C57BL, Mice, Ethanol, Morphine, Alloxan, Cyclic AMP, Animals, Hypoxia, Brain, Ether
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