Yoshimasa Takeda

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PURPOSE Temporary brain ischemia occurring during surgery under general anesthesia may induce the death of neuronal cells and cause severe neurological deficits. On the other hand, it is not clear whether μ-opioid receptor agonists promote ischemic brain injury. It is known that duration of ischemic depolarization affects the degree of neuronal damage.(More)
The predictive value of increase in cerebral blood flow (CBF) was examined to detect hyperbaric oxygen (HBO(2))-induced electrical discharge in artificially ventilated rats at three PaCO(2) levels under 5 atmospheric pressures. The possible involvement of NO production in the mechanism of the increase in CBF was also assessed by measurement of major NO(More)
Hyperbaric oxygen (HBO(2)) exposure induces increases in cerebral blood flow (CBF) and extracellular concentrations of nitric oxide (NO) that precede the appearance of central nervous system toxicity, which may manifest as convulsions. To elucidate the origins of NO production during HBO(2) exposure, we examined the effects of the selective neuronal NO(More)
To examine the usefulness of diffusion-weighted imaging for detecting neuronal damage following ischemia, dynamic changes in diffusion-, T1- and T2-weighted images of rats subjected to 10 min of 4-vessel occlusion and of humans who had suffered 10-20 min of cardiac arrest were observed. In rats, no remarkable alteration was observed on day 1. On day 3,(More)
Previous studies have indicated that prolonging the onset of ischemic depolarization reduces neuronal damage. However, the relationship between the duration of ischemic depolarization and its histological outcome has not been quantitatively evaluated. Rats were anesthetized (with 1% halothane), intubated, and placed in a stereotaxic frame. Direct current(More)
Induced ischemic tolerance in rat hippocampus was investigated in a forebrain ischemia model of repeated 4-vessel occlusion (4-VO). Ischemic insult variability was reduced by the use of dc potential measurements to determine the duration of ischemic depolarization in hippocampus. The results demonstrate a depolarization threshold for ischemic injury to CA1(More)
To try to determine the cause of hyperintensity of T1-weighted MR images that occurred on and after day 7 following transient cerebral ischemia, dynamic changes in T1-weighted images and histology of rats subjected to 20 min of 4-vessel occlusion were observed. T1-weighted images showed no remarkable alteration on days 1 and 3, although high signal(More)
Although propofol and thiopental are commonly used as neuroprotective agents, it has not been determined which is more neuroprotective. This study was designed to quantitatively evaluate the neuroprotective effects of thiopental, propofol, and halothane on brain ischemia by determining P50, ischemic time necessary for causing 50% neuronal damage. Gerbils(More)
Suppression of peri-infarct depolarizations (PIDs) is one of the major mechanisms of hypothermic protection against transient focal cerebral ischemia. Previous studies have shown the lack of hypothermic protection against permanent focal ischemia. We hypothesized the lack of hypothermic protection was due to the poor efficacy in suppression of PIDs. To(More)
To elucidate the mechanism by which hyperbaric oxygen (HBO2) induces electrical discharge, changes in the extracellular concentrations of GABA and glutamate were measured every 5 min using a microdialysis technique in rats during a period of exposure to HBO2 (5 atm abs). Electrical discharge was observed at 28 +/- 4 min after the onset of exposure. Though(More)