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Biomedical subjects

S Sakaki

Publications and source records attributed to S Sakaki.

204 records · Page 12Linked to original sources
PubMedDate not supplied

Early detection of cerebral ischemic lesion using diffusion-weighted MRI.

We performed serial diffusion-weighted imaging (DWI) in a patient with right middle cerebral arterial occlusion using 1.0 T MRI. The initial DWI demonstrated suppression of water diffusion in the gray matter in the ischemic lesion as a high signal area 4 h after stroke onset, when T2-weighted imaging failed to detect any parenchymal injury. Repeat DWI 9 h after onset demonstrated the whole infarct, whereas it was not demonstrated by T2-weighted imaging until 48 h. Furthermore, the regional apparent diffusion coefficient (ADC) had already decreased significantly in both the gray and white matters of the ischemic lesion 4 h after onset, even though hyperintensity was not visible in the white matter on the DWI. The features in this case indicate that DWI in conjunction with the assessment of regional ADC can provide important information regarding the evolving infarct at a very early stage even when a relatively low tesla clinically available MRI unit is used.

Brain Ischemia↗
PubMedDate not supplied

Biological defence mechanism in the pathogenesis of prolonged cerebral vasospasm in the patients with ruptured intracranial aneurysms.

We examined the relationship between the biological protective mechanisms of scavengers and free radicals that are elicited by subarachnoid hemorrhage (SAH) in the pathogenesis of prolonged vasospasm following ruptured intracranial aneurysm. The study included 25 patients treated by early surgery (within 72 hours after SAH). Lipid peroxides concentrations and the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px) in the cerebrospinal fluid (CSF) were measured. The concentration of lipid peroxides increased significantly more (p less than 0.05) during the first 4 days after SAH in patients with symptomatic vasospasm than in those without. Patients with symptomatic vasospasm had a marked decrease in SOD activity on Days 3 and 4 followed by a gradual decrease, whereas the patients without spasm showed little change (difference between the groups, p less than 0.05). There was a significant difference in catalase activity reversal to SOD activity, but no difference in GSH-px activity. Thus, correlation was close between the increased lipid peroxides concentration and the decrease in SOD activity in CSF (p less than 0.05), suggesting an important mechanism in the pathogenesis of vasospasm.

Adult↗
PubMedDate not supplied

Cation activities in reversible ischemia of the cat brain.

In normothermic anesthetized cats cerebral blood flow was interrupted completely for one hour by arterial clamping and induced hypotension. The effect of ischemia on the ionic gradients of the cerebral cortex was assayed by determining total cortical electrolytes and by recording the activities of extracellular potassium ([K+i1e) and subarachnoid sodium ions ([Na+])s) with ion-sensitive electrodes. During ischemia [K+]e increased from 3.3+/-0.3 to 56+/-5.4 mEq per liter (means+/-SE) and [Na+]s decreased from 133+/-3.8 to 53+/-5.8 mEq per liter. When the brains were recirculated with blood after one hour's ischemia, [K+]e and [Na+]a gradually returned to normal within 45 minutes. The calculated intracellular uptake of sodium during ischemia amounted to 139 mEq per kilogram dry weight, whereas the intracellular release of potassium was only 64 mEq per kilogram. The increase in intracellular cation was accompanied by a movement of water from the extracellular into the intracellular compartment, causing a reversible shrinkage of the extracellular space from 18.9 to 8.5 vol %. The changes in ionic gradients were related to the development and resolution of ischemic brain swelling, and to the elctrophysiological events during and after ischemia.

Animals↗