The possibility that cerebral ischemia or cerebral hypoxia may initiate a series of free radical reactions in brain tissue lipid constituents was explored by measuring sequential changes in chemiluminescence values and energy metabolism during brain hypoxia in the rat. Brain hypoxia was induced by means of arterial hypoxemia (PaO2 17-22 mmHg), normocapnia (PaCO2 28-38 mmHg) and normotension (MABP 100-140 mmHg). To obtain lowered PaO2, 4% O2--96% N2 mixed gas was used. Analysis of the chemiluminescence spectra for the purpose of luminous mechanism investigation was again attempted. No peroxidation occurred in the pre-hypoxic state since there were no photon counts. Chemiluminescence began to rise in the hypoxic state and remained at a high value in the post-hypoxic state. Specifically in the hypoxic state, the 3 min period showed 231 +/- 35 counts/10 sec X g (n = 5) and the 5 min period showed 154 +/- 62 (n = 19) counts/10 sec X g. In the post-hypoxic state, the 5 min period showed 217 +/- 79 counts/10 sec X g (n = 9) and the 30 min period showed a decrease similar to the pre-hypoxic state. The chemiluminescence spectroanalysis showed five peaks in wavelength at 480 nm, 520-530 nm, 570 nm, 620-640 nm and 680-700 nm. Sequential changes in energy metabolism revealed that hypoxia caused marked brain lactic acidosis, an increase in both ADP and pyruvate, and a fall in glucose. However, all metabolites recovered at 30 min in the post-hypoxic state, which suggests this was reversible brain hypoxia. Sequential changes in chemiluminescence values and energy metabolism imply the occurrence of free radical reaction in the hypoxic and post-hypoxic brain. The spectroanalysis reveals the luminous mechanism as follows: 1 delta g + 1 delta g----23O2 + h mu
Adenosine Diphosphate Animals