[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.