BRAIN ENERGY METABOLISM OF CEREBRAL ISCHEMIC MICE AND THE EFFECTS OF SOME DRUGS

Two simple cerebral ischmic models of mice were used for studing brarn energy metabolism and the effects of drugs Model one is partial occlusion of the left carotid artery and total occlusion of the right one including the vagus. The behavior of the animals appeared splaying of the contralateral extremities, circling around counterelockwisely and in a comatose motionless state Following the designated ischemic time. the animals were put into liquid N₂ Model two is decapitation induced ischemia of mouse brain The whole ammal (control) and the severed head were rapidly frozen in liquid nitrogen 0, 10, 30, 60 s after decapitation Brain samples were powdered at liquid N₂ temperature, extracted and determined for ATP, phosphocreatine (Pcr) and lactic acid (LA) The data from model one indicate that after an ischemic period of 10 rain. brain LA level increased significantly compared with values from the sham operated group, while no significant alteration was observed in brain ATP, and Pcr level Al 180 min of tschemia, levels of ATP and Pcr were constderably reduced while LA level mcreased significantly The degree of symptoms induced by brain ischemia showed good correlation with brain energy metabolism In model 2 brain LA level was found to be increased, while ATP and Pce levels decreased after whole brain ischemia However, brain ATP and Per level were increased and LA level was decreased significantly in the normal and ischemic an mal after administration of phenobarbital (225 mg/kg ip) LA level decreased lognifi cantiy niticantry in the unischemic mice treated with Rb₁ (100 mg/kg 1p) it is indicated thar boti models or cerebral ischelnia were simple and sensitive methods for studying brarn tschemia Nimodipme nifedipine, nicarlipine, Rb₁, panaxdiol, and panaxtriol al cyhibrted brain protection effect in mics.