The relationship between thermoreception, hormonal secretion and muscular activity was studied. 6 men swam 60 min in 21, 27 and 33 degrees C water at a speed requiring 68% of VO2 max (determined in 27 degrees C water). Rectal temperature increased in 33 degrees C (1.3 +/- 0.2 degrees C, mean and S.E.) and 27 degrees C (0.7+/- 0.1 degrees C) expts. but decreased in 21 degrees C expts. (0.8 +/- 0.3 degrees C). Changes in esophageal and muscle temperatures parallelled changes in rectal temperature. Plasma noradrenaline was higher in 33 degrees C than in 27 degrees C expts. and growth hormone, cortisol and glucagon concentrations increased in 27 degrees C and 33 degrees C expts. only. Insulin concentrations were uniformly depressed during swimming at the different water temperatures. In 21 degrees C expts. noradrenaline and adrenaline concentrations were higher than in 27 degrees C expts. VO2, carbohydrate combustion and peak lactate were slightly lower in 33 degrees C expts. Plasma glucose decreased slightly and FFA and glycerol concentrations increased identically in all expts. Heart rate increased continuously during swimming in 27 degrees C and 33 degrees C expts., but not in 21 degrees C expts. In conclusion the rise in body temperatures normally observed during exercise enhances the exercise induced increases in the plasma concentrations of noradrenaline, cortisol, growth hormone and glucagon. Decreased body temperatures may elicit catecholamine secretion as a direct consequence of thermoreception. Shivering may account for previously observed decreases in insulin secretion during cold stress but not for increases in cortisol and growth hormone.

SUMMARY 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 (PaO 2 17-22 mmHg), normocapnia (PaCO 2 28-38 mmHg) and normotension (MABP 100-140 mmHg). To obtain lowered PaO 2 , 4% O 2 -96% N 2 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-g (n = 5) and the 5 min period showed 154 ± 62 (n = 19) counts/10 sec-g. In the post-hypoxic state, the 5 min period showed 217 ± 79 counts/10 sec-g (n = 9) and the 30 min period showed a decrease similar to the pre-hypoxlc state. The chemiluminescence spectroanaljsis 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 posthypoxic brain. The spectroanalysis reveals the luminous mechanism as follows: 'Ag + 'Ag -» 2 3 O 2 + h/x Stroke Vol 15, No 6, 1984 IN RECENT YEARS THE AUTO-OXIDATION of unsaturated fatty acids has been suggested as one of the primary factors in the acute stage pathology of the ischemic or hypoxic brain.'" 4 It has been difficult to detect the free radical reactions and further uncertainties remain with regard to the correlation between the period during which lipid peroxidation occurs and the energy metabolism of the brain.5 " 9In the present study, we have followed the sequential changes of chemiluminescence and energy metabolism during a period of both induced hypoxia and oxygen resupply by using supratentorial tissue of hypoxic rat brain (PaO 2 , 17-22 mmHg).Chemiluminescence analysis is a new technique in which the propagation or termination of free radical reaction is thought to appear when singlet oxygen has been transmitted to the triplet oxygen.10 " 15 The results obtained using this new technique were found to be in agreement with the free radical reaction as determined simultaneously from the perspective of energy metabolism. Experimental Materials and MethodsFor the purpose of this study, 142 male Wister rats (250-280 g) were used. In the chemiluminescence value study, 9 rats were sacrificed at pre-hypoxia, 5 at hypoxia-3 min, 19 at hypoxia-5 min, 9 at post-hypoxia-5 min, a...

SUMMARY 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 (PaC>217-22 mmHg) with normocapnia (PaCO 2 28-38 mmHg) and normotension (MABP 100-140 mmHg). 4%C>2-96%N 2 mixed gas was used to obtain the lowered PaO 2 .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 spectroanalysis shows that vitamin E arid betamethasone act on the late chain reaction following hydroperoxide and mannitol acts on the early reactiongeneration of active Oxygens. Stroke Vol 16, No 4, 1985 FIFTEEN YEARS AGO we performed a direct operation on an aneurysm of the right middle cerebral artery of a 50 year-old female, during which 50 minute temporary vascular occlusion at normothermia was unavoidable. Despite the occlusion, the postoperative recovery was uneventful and she was discharged without neurological symptoms. These events led us to suspect that the mannitol which had been administered to decrease intracranial pressure during the operation and prior to vascular occlusion had worked to prevent the development of cerebral infarction, which had been expected due to the lengthy vascular occlusion. Since then, we have been investigating the effects of mannitol on cerebral function using various animal models 12 for producing cerebral infarction in the dogs. Using one variation of the canine infarction model 3 has been demonstrated the cerebral protective effects of mannitol using brain electrical activity as an index of the brain's functional state.4 " 6 Moreover, the protective effects of related substances have also been demonstrated, including those of vitamin E, 7 glucocorticoid and perfluorochemicals administered with the mannitoi. 8 Recently, we have used a chemiluminescence method 9 "12 together with a hypoxic rat brain preparation, and found a significant increase in photon emission, which is known to be a demonstration of a propagation in free radical reaction. In the present study, we have investigated the effects on the hypoxic brain of various cerebral protective drugs, including vitamin E, 7 -l3 be- 2 '" 25 we have performed chemiluminescence spectral analysis before and after drug administra...