[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.
D000496:Alloxan / Q000627:therapeutic use; D000818:Animals; D001923:Brain Chemistry; D000242:Cyclic AMP / Q000032:analysis*; D000431:Ethanol / Q000627:therapeutic use; D004986:Ether / Q000627:therapeutic use; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000517:prevention & control; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009020:Morphine / Q000627:therapeutic use
D004986:Ether; D000431:Ethanol; D000496:Alloxan; D009020:Morphine; D000242:Cyclic AMP
Uvelichenie soderzhaniia tsAMF v kletkakh golovnogo mozga mysheĭ pri ishemii i tormozhenie étogo éffekta pod vliianiem nekotorykh biologicheski aktivnykh soedineniĭ.