1993 Fiscal Year Final Research Report Summary
CEREBRAL DAMAGE ON EXPERIMENTAL BRAINISCHEMIA SEQUENTIAL CHANGE OF CELLULAR REACTION
| Project/Area Number |
04454354
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | HIROSAKI UNIVERSITY |
|---|
Principal Investigator |
KOYA Goyo HIROSAKI UNIVERSITY SCHOOL OF MEDICINE PROFESSOR, 医学部, 教授 (20091605)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Yasuji HIROSAKI UNIVERSITY SCHOOL OF MEDICINE ASSOCIATE PROFESSOR, 医学部, 助教授 (70126465)
MORI Fumiaki HIROSAKI UNIVERSITY SCHOOL OF MEDICINE RESEARCH ASSOCIATE, 医学部, 助手 (60200383)
|
|---|
| Project Period (FY) |
1992 – 1993
|
| Keywords | ISCHEMIA / GLOBAL AND FOCAL / NO OPENED CRANIUM ON OPERATION / PENUMBRA / SAPINAL ROOT GANGLIA / HEMORRHAGE / SPINAL CORD / PARAPLEGIA |
|---|
| Research Abstract |
Focal brain ischemia induced in rats by occulsion of an intracranial artery is a widewly used paradigm of human brain infarct. Details of the structural changes that develop in either the human or the rat brain at various times after occulsion of an intracranial artery are incompletely characterized. We are studied, in adult rat on inherited controlled for various kind of Wistar- and SHR.SR or SHR.SP and SD rats, structureal alterations involving the cerebral hemisphere ipsilateral to an arterial occulsion, at intervals ranging from 30 min to 7 days. The gross pattern of the brain lesion and the maturation of neu ronal changes typical of a brain infarct have a predictable progression. Focal brain ischemia of up to 6-hour duration does not induce coagulation necrosis.
The photosensitizing agent, such as Photofrin II, cause necrosis of cells(neoplastic as wellas normal), probably by promoting formation of free radical species, on photoactivation, We completed a time-dependent study of the effects that photoactivatig Photofrin II may have on normal rat brain and reported early injury to astrocytes and secondarily, to the microvasculature and the neurons.
Among of the short-term on postoperation of cerebral infarct subtle hemohrrage localized in spinal root ganglion have been involed at level of lummbal and cervical. The ganglia hemohrrage caused by incresed CSF pressure induced after series of increased cranial pressure and after with that few case was involing focal hemohrrge of characteristic in spinal cord itself. Any information of spinal enviromentalinvolved at the time may be clinically given a soluble process for syringomyelia.
|
