Chemiluminescence in hypoxic brain--the second report: cerebral protective effect of mannitol, vitamin E and glucocorticoid.

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Abstract
The effect of vitamin E, betamethasone and mannitol upon a series of pathological free radical reactions within hypoxic brain tissue was evaluated by the chemiluminescence method. Hypoxia was induced by arterial hypoxemia (PaO2 17-22 mmHg) with normocapnia (PaCO2 28-38 mmHg) and normotension (MABP 100-140 mmHg). 4% O2-96% N2 mixed gas was used to obtain the lowered PaO2. In the untreated group, increased chemiluminescence was measured in the hypoxic state and the early stage of the initial post-hypoxic state. In the groups administered vitamin E, betamethasone, mannitol and a combination of them reduced chemiluminescence was detected. To explore the reaction stage at which the drugs act in lipid peroxidation, chemiluminescence spectra was analyzed using the brain homogenate with the drugs added. Intensity peaks of the spectra were around at 480, 520-530, 570, 620-640, 680-700 nm before addition of the drugs. All the intensity peaks diminished after addition of vitamin E and betamethasone, but very little decrease occurred after mannitol. The lowered chemiluminescence value may indicate the free radical scavenging action of vitamin E, betamethasone and mannitol in vivo. Chemiluminescence spectrum analysis shows that vitamin E and betamethasone act on the late chain reaction following hydroperoxide and mannitol acts on the early reaction--generation of active oxygens.