Exercise-induced "arterialization" of venous blood in some schizophrenics: a further note on possible microcirculation disturbances.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Andou.
Explore the source record for details and available documents.
Bindings of glutamate receptor agonists and related modulators were investigated in 10 discrete tissues from gerbil brain using a biochemical technique. There appeared considerable discrepancies, in respect of intrahippocampal profiles, from reported data by autoradiography on rat brain. In the gerbil, an almost equivalent level of N-methyl-D-aspartate (NMDA)-displaceable [3H]glutamate binding was found in field CA1 and the dentate gyrus, while approx 30% less in field CA3, a profile which was strikingly similar to that of (+)-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]-cycloheptene-5,10-imin e maleate (MK-801) or of [3H]glycine. [3H]Kainate binding was highest in the dentate gyrus followed by field CA3 and then field CA1, the ratio of the highest to the lowest being 3 to 2. Binding of [3H]DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) differed, to a certain extent, from that of [3H]kainate and showed the dentate gyrus followed by field CA1 and then field CA3 in the rank order of decreasing binding. Taking together, intrahippocampal localization of glutamate receptor subtypes in the gerbil, when analyzed with a biochemical binding assay, looks to be less region selective than the distribution obtained on autoradiography in the rat. Thus, it is likely that these different distribution profiles show different status of receptor function respectively, or are due merely to species difference.
It has not been discussed whether transient forebrain ischemia of 5-min duration, which is a model frequently used to evaluate pharmacological protection against ischemic injury, is an optimal model in the CA1 field of this animal whose brain temperature is maintained at normothermic levels. The temperature of the brain during an ischemic insult strongly affects the extent of the resulting neuronal injury. If the brain temperature is not regulated, it usually falls in the gerbil by 2 degrees-4 degrees C during 5-min ischemia. However, the brain temperature during ischemic insult was not regulated in many previous studies. In the present study, the effects of transient (1 to 5 min) forebrain ischemia on the development of neuronal degeneration in hippocampal regions of the gerbil whose brain temperature was maintained at 37 degrees C were examined. In the CA1 field of the hippocampus, transient ischemia of 3- and 4-min duration caused almost the same maximal damage (88%-91% neuronal loss) as observed in the gerbils subjected to 5-min ischemia. Transient ischemia of 2- and 2.5-min duration provoked substantial neuronal damage in 25% and 55% of experimental gerbils, respectively. These results indicate that 5-min bilateral forebrain ischemia is more than is necessary to examine ischemia-induced neuronal degeneration in hippocampal CA1 field of the gerbil whose brain temperature is maintained at normothermic levels. In the normothermic gerbil brain, an ischemic period of 3-min already induces extensive neuronal death in the CA1 and, thus, constitutes a sensitive model to evaluate faint protective effects of drugs against ischemic injury in the normothermic gerbil.
Ischemia-induced selective neuronal injury to field CA1 is not attributable to selective glutamate release in field CA1 during ischemia. Excessive release of glutamate has been proposed to play a major role in ischemia-induced selective neuronal death in field CA1 of the hippocampus. It is well known that, following carotid arterial occlusion of 5 min duration in the gerbil, the pyramidal neurons in field CA1 show delayed neuronal death, whereas the neurons in field CA3 do not show any neuronal degeneration. In the present study, we measured the levels of released glutamate during ischemia in field CA1 and field CA3, separately, and evaluated whether there are subregional differences in the concentration of released glutamate which could be a satisfactory explanation for the selective vulnerability of hippocampal neurons to ischemia. Extracellular glutamate levels were significantly increased during ischemia in both field CA1 and field CA3. No significant differences were detected in the time-course of change in glutamate release and the levels of glutamate between field CA1 and field CA3. This result indicates that the increased glutamate levels do not play a pivotal part in the detrimental effect of glutamate during 5-min ischemia. Some differentiated post-synaptic organization may act as a crucial factor in the development of ischemia-induced selective neuronal death in the gerbil hippocampus.
We examined the effect of transient forebrain ischemia of 2-, 3-, 4- and 5-min duration on the development of delayed neuronal death in field CA1 of the hippocampus in the gerbil whose brain temperature was maintained at 37 degrees C. Transient ischemia of 3- and 4-min duration caused almost the same maximal damage in field CA1 as observed in the gerbils subjected to 5-min ischemia. A detrimental factor inducing delayed neuronal death in field CA1 may be already set up during the first 3 min after the onset of ischemia in the gerbil whose brain temperature is maintained at normothermic levels.
The completeness of brain ischemia with a multi-arterial clamping method in dogs was examined using EEG, evoked potentials (EPs) and vessel staining with Evans blue. EEG was monitored by bipolar parietal lead. EPs stimulating electrodes were inserted into the first thoracic (T1) epidural space and recording electrodes into the C2 epidural space, brain stem and cerebral cortex. EPs were measured at 30 s intervals with 50 measurements each time using 3.0 mA current of 100 microseconds duration. In dogs in which brain ischemia was brought about by ventricular fibrillation (VF group, n = 5) EEG disappeared within 40 s in all dogs and the amplitudes of EPs at the C2 spinal cord, brain stem and cerebral cortex after 10 min ischemia were 57%, 0% and 0%, respectively. In the dogs in which a multi-arterial clamping method (clamping internal thoracic arteries, brachiocephalic trunk and left subclavian artery while lowering systolic arterial pressure (AP) below 50 Torr) was used (AC group, n = 5) EEG was still recognizable at 5 min in 2 dogs and the amplitudes of EPs at the C2, brain stem and cerebral cortex at 10 min ischemia were 103%, 53% and 0%, respectively. Stainings with Evans blue were observed in all soft tissue at and below thoracic level, entire intervertebral venous plexus, venous sinuses of cranial dura mater and spinal cord below the lower part of cervical region. Bright red fluorescence by Evans blue was observed microscopically in the vessels of the spinal cord, brain stem and cerebrum (1 dog only). In conclusion a multi-arterial clamping method with arterial hypotension brings about only incomplete brain ischemia.
It has been proposed that neuronal hyperexcitability during postischemic chronic stage mediates delayed neuronal death in the hippocampal CA1 region. In the present study, multiple-unit spike discharges were continuously recorded from hippocampal CA1 neurons of the awake Mongolian gerbil for 5 days after 5 min of ischemia. Before ischemia, CA1 neurons showed burst-like spike discharges (so-called complex spikes). Spike discharges disappeared 8-40 s after the onset of 5-min ischemia and reappeared 5-30 min after recirculation. The frequency of discharges gradually increased but did not return to the preischemic level. The amplitude of the spike discharges was smaller than that recorded before ischemia and the number of spikes composing the burst-like discharges diminished. CA1 neurons did not show any hyperexcitability for 5 days. However, histological examinations revealed widespread neuronal death in the CA1 region. These results indicate that the delayed neuronal death in the hippocampal CA1 region is induced without postischemic neuronal hyperexcitability.
Explore the source record for details and available documents.
Lactate, glycerol, adrenaline, and noradrenaline in venous blood following 400 m and 3000 m runs were measured in 6 untrained male students, 5 female handball players, 6 female sprinters and 6 female long-distance runners. Physical performance in the two events by the untrained males was the same as for the female handball players, but was less than that by the female sprinters and female long-distance runners. Peak blood lactate levels obtained after 400 m sprinting, and glycerol concentration following the 3000 m run were not significantly different between the untrained males and the female handball players. On the other hand, both peak blood lactate concentrations after 400 m sprinting for female sprinters and peak blood glycerol levels following a 3000 m run for female long-distance runners were significantly higher than those in the untrained male subjects. In both runs there was no significant difference in adrenaline and noradrenaline between the untrained male group and the female handball players. These results suggest that blood lactate in a 400 m run, and glycerol in a 3000 m run might be a reflection of physical performance level but not of sex difference.
The normal development of the spinal cord from the fetal period to infancy was studied by ultrasonography (US) with a 7.5 MHz transducer. Longitudinal and transverse sections of the spinal cord were clearly observed. The sagittal and transverse diameters of the spinal cord increased with age. In order to evaluate disorders of the spinal cord precisely, it is necessary to clarify the normal features as well as the normal development of the spinal canal and cord, and the surrounding structures. US with such a high frequency transducer will be the most suitable for this purpose.
This clinical study was undertaken in order to evaluate the effect of CDDP on 43 patients with far-advanced or recurrent carcinoma of the gastrointestinal tract. For all these patients, CDDP at 100 mg/m2 had been administered by continuous intravenous infusion for 24 hours and repeated one to seven times at an interval of 3 to 4 weeks. The effect of this therapy was assessed according to the criteria of clinical evaluation of chemotherapy for solid cancers by Koyama and Saito. The response rate for both complete and partial response was 27.9% among all 43 patients, including 47.1% (8/17) for gastric cancer, 33.3% (1/3) for esophageal cancer, 25.0% (1/4) for hepatocellular carcinoma, 25.0% (1/4) for carcinoma of the gallbladder or bile duct, 20.0% (1/5) for pancreatic cancer and none (0/10) for colorectal cancer. In particular, a good response rate of 37.5% (3/8) was obtained for patients with recurrent tumor and one of 33.3% (6/18) for those with palliative resection of the primary tumor, which was much higher that the rate of 17.6% (3/17) for those without resection. As for the side effects of CDDP therapy, gastrointestinal symptoms were most frequently found in 78.3% of patients followed by bone marrow suppression in 15.2%, and abnormalities of hepatic and renal function in 4.3% and 4.3%, respectively. Consequently, 24-hour continuous intravenous infusion of CDDP was considered to be effective for far-advanced or recurrent carcinoma, especially in cases of gastric cancer.