Project/Area Number |
13671570
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | Gifu University |
Principal Investigator |
IIDA Hiroki GIFU UNIVERSITY SCHOOL OF MEDICINE, DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE MEDICINE, ASSOCIATE PROFESSOR, 医学部, 助教授 (30159561)
|
Co-Investigator(Kenkyū-buntansha) |
DOHI Shuji GIFU UNIVERSITY SCHOOL OF MEDICINE, DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE, PROFESSOR, 医学部, 教授 (40155627)
|
Project Period (FY) |
2001 – 2003
|
Project Status |
Completed (Fiscal Year 2003)
|
Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
Keywords | Aortic cross-clamping / Cerebral vessel / Mechanism / Thromboxane A_2 / Free radical / Milrinone / Colforsin daropate / Prostaglandin E_1 / トロンボキサンA2 / コルフルシンダルパート / プロスタグランジンE1 / 脳 / 脊髄 / 微小循環 / トロンボキサンA2受容体 / 大動脈遮断 / 解除 |
Research Abstract |
Pentobarbital anesthetized rabbits were prepared for measurement of cerebral pial vessel diameter in a cranial window preparation. We investigated the experiments according to following protocols. (1)We studied the effect of aortic clamping and declamping on cerebral pial vessel diameter. Although infrarenal aortic cross-clamping did not affect pial vessel diameter, release of a 20-min aortic cross-clamp caused pial arterioles to dilate and then constrict. A significant constriction persisted for at least 60 mm. (2)To clarify the mechanism of changes in cerebral microcirculation during and after abdominal aortic cross-clamping, we examined whether seratorodast, a thromboxane (Tx) A2 receptor antagonist, or edaravone, a free radical scavenger, would affect the respose observed after abdominal aortic cross-clamping. Both seratrodast and edaravone significantly attenuated the constriction of pial arterioles. Thus such vasoconstriction is partly induced via a washout of the TxA2 and free radicals produced in the ischemic region during and after cross-clamp release. (3)We investigated the effect of vasoactive agents such as milrinone, colforsin daropate, or prostaglandin E1 on arteriolar constriction observed after abdominal aortic cross-clamping. Clinical dose of milrinone and colforsin daropate but not prostaglandin El attenuated the constriction of pial arterioles after cross-clamp release.
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