Contribution α2B adrenoceptor activation to cerebral vasospasm and cerebral infarction
Project/Area Number |
16591561
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | Kitasato University |
Principal Investigator |
OKAMOTO Hirotsugu Kitasato University, Anesthesiology, Associate Professor, 医学部, 助教授 (50224077)
|
Project Period (FY) |
2004 – 2005
|
Project Status |
Completed (Fiscal Year 2005)
|
Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
|
Keywords | central nervous system / Sympathetic nerve / cerebral blood flow / cerebral infarction / α-receptor / 脳血管スパズム |
Research Abstract |
1)Reperfusion following regional ischemia : Acute and Chronic rat model : We examined the cerebral blood flow via cranial window. Reperfusion was made two hours after occluding MCA. 72-96 hr later we evaluated infract area with TTC and HE staining. We found that high concentration of dexmedetomidine which activates alpha 2B adrenoceptor aggravates brain damage by cerebral ischemia. Results were clearer in chronic rat model. 2)Subarachnoid hemorrage : Cerebral vasospasm rat model : We made acute cerebral vasospasm rat model, and found decreases in cerebral blood flow and diameter. However, the survival rate is rather low and it was difficult to interpret data. 3)Pharmacological approach : Dexmedetomidine-induced aggravation was attenuated by the relatively selective alpha 2B antagosist, yohimbine but not by rauwolscine which is selective alpha 2C antagosist. Therefore, it is suggested that alpha 2B adrenoceptor plays an important role in brain damage caused by cerebral vasospasm and cerebral ischemia.
|
Report
(3 results)
Research Products
(6 results)