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K Takakura

Publications and source records attributed to K Takakura.

507 records · Page 29Linked to original sources
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Identification and quantitative analysis of hydroxy-eicosatetraenoic acids in rat brains exposed to regional ischemia.

To clarify possible roles in the pathogenesis of ischemic brain edema, identification and quantitative analysis of hydroxy-eicosatetraenoic acids (HETEs) in rat brains exposed to middle cerebral artery occlusion were carried out using high-performance liquid chromatography. Rat brain sampling was done by in situ freezing 24 and 72 hours after occlusion. Only a small amount of 15-HETE was found in control rat brains. Twenty-four hours after ischemia, 11-HETE appeared, and the amount of 15-HETE tended to increase. Seventy-two hours after ischemia, when brain edema reached its maximum, 5-, 8-, 9-, 11-, 12-, and 15-HETEs were identified, and the amounts of all HETEs except 8- and 12-HETE were significantly increased. The detection of 5-HETE in ischemic rat brain indicates the simultaneous production of leukotrienes in the same brain area. The above results support the view that lipoxygenase products may play significant roles in the formation of ischemic brain edema.

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Effect of cervical spinal cord stimulation (cSCS) on cerebral glucose metabolism and blood flow in a vegetative patient assessed by positron emission tomography (PET) and single photon emission computed tomography (SPECT).

This paper presents, for the first time, assessments of cerebral glucose metabolism and cerebral blood flow before and after cervical spinal cord stimulation (cSCS) in a vegetative patient. Regional cerebral metabolic rates for glucose (rCMRglc) were measured with positron emission tomography and 18F-fluoro-2-deoxy-D-glucose. Regional cerebral blood flow (rCBF) was determined with single photon emission computed tomography and N-isopropyl p-123I-iodoamphetamine. Global CMRglc in the patient was less than one-third of that in normal control subjects. An increase in rCMRglc after one week of cSCS was observed in the cerebral cortex, predominantly on the right side, where the baseline level of rCMRglc before cSCS was more severely depressed. The pattern of increase in rCBF was almost the same as that in rCMRglc. The results suggest that cSCS activates glucose metabolism and that this is followed by an increase in cerebral blood flow.

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