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Biomedical subjects

K Munekata

Publications and source records attributed to K Munekata.

9 recordsLinked to original sources
PubMed1988

Effect of autologous clot embolism on regional protein biosynthesis of monkey brain.

Focal cerebral ischemia was produced in monkeys by injection of autologous clots into the left internal carotid artery. Regional protein synthesis was studied 2 hours after embolism by autoradiographic and biochemical evaluation of [3H]phenylalanine incorporation into brain proteins, and the results were correlated with electrophysiologic (electroencephalogram, evoked potentials) and light microscopic observations. Ischemic territories were clearly identified on autoradiograms as sharply demarcated areas with reduced radioactivity. The localization of regions with reduced protein biosynthesis correlated with the early postembolic suppression of evoked potentials but not with the (improved) functional state and the morphologic alterations at the end of the experiment. Suppression of amino acid incorporation, in consequence, is a long-lasting event that allows documentation of the initial embolic impact for at least 2 hours irrespective of the subsequent recovery process.

Animals↗
PubMed1985

Intracerebellar hemorrhage due to cerebellar hemangioblastoma.

A rare case of a bleeding from a cerebellar hemangioblastoma is described. The tumor was diagnosed preoperatively with a computed tomography scan and a vertebral angiogram. The characteristic computed tomography scan findings and probable mechanism of bleeding are discussed.

Cerebellar Diseases↗
PubMed1985

Delayed intracerebral hemorrhage after ventriculoperitoneal shunt.

A serious intracerebral hemorrhage occurred as a result of a measurement for grip power performed on the 7th postoperative day of a ventriculoperitoneal shunt. This type of delayed intracerebral hemorrhage after the placement of a ventriculoperitoneal shunt has not been described in the literature. The increased intracranial venous pressure produced by Valsalva's effect induced this complication, which is also considered to be the same mechanism as traumatic delayed intracerebral hemorrhage.

Adolescent↗
PubMed1979

[A case of accessory middle cerebral artery associated with internal carotid artery aneurysm (author's transl)].

A case of accessory middle cerebral artery associated with internal carotid artery aneurysm was reported. A 50-year-old female was admitted to our hospital with complaints of headache, nausea, vomiting and conciousness disturbance. Lumbar puncture showed bloody CSF. Right carotid angiogram revealed saccular aneurysm of the internal carotid-posterior communicating artery and accessory middle cerebral artery originating from the horizontal portion of the right anterior cerebral artery. No other vascular lesion was observed on other angiograms. Operation was performed 2 days after admission. The neck of the aneurysm was clipped. Postoperative aseptic meningitis was cured by frequent lumbar punctures, and her course was uneventful. The etiological hypothesis of these cerebral vascular anomalies was briefly discussed.

Carotid Artery Diseases↗
PubMedDate not supplied

Effect of 5-minute ischemia on regional pH and energy state of the gerbil brain: relation to selective vulnerability of the hippocampus.

Adult male gerbils were submitted to 5-minute cerebral ischemia by bilateral carotid artery occlusion. At the end of ischemia and at various recirculation times ranging from 15 to 120 minutes, brains were frozen in situ and the regional distribution of ATP, glucose, and tissue pH was studied on coronal cryostat sections by bioluminescent and fluoroscopic techniques. During ischemia ATP was completely depleted, glucose decreased to less than 10% of control, and regional tissue pH decreased from 7.04-7.09 to about 6.0. After the beginning of recirculation tissue pH and the regional content of metabolites exhibited a triphasic course. After 15 minutes pH returned to or even above normal, and ATP- and glucose-induced bioluminescence normalized. However, there was a secondary deterioration of both tissue acidosis and the metabolic state after 30 minutes. After longer recirculation times changes again improved and returned to normal within 2 hours. These changes were similar in all brain regions with the exception of the CA1 sector of the hippocampus, where the transient normalization of tissue pH was absent after 15 minutes of recirculation. This finding is in line with the previously observed microcirculatory insufficiency of this area and demonstrates that the CA1 sector of the hippocampus suffers more pronounced postischemic acidosis than other less vulnerable regions of the brain.

Animals↗