2006 Fiscal Year Final Research Report Summary
Development of the pencil-typed imaging system to evaluate the disturbance of coronary microcirculation during coronary ischemia-reperfusion injury
| Project/Area Number |
16300164
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Biomedical engineering/Biological material science
|
|---|
| Research Institution | Kawasaki Medical School |
|---|
Principal Investigator |
YADA Toyotaka Kawasaki Medical School, School of Medicine, Assistant Professor, 医学部, 講師 (00210279)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KATSURA Masashi Kawasaki Medical School, School of Medicine, Assistant Professor, 医学部, 講師 (80204452)
OKUMA Seitaro Kawasaki Medical School, School of Medicine, Professor, 医学部, 教授 (30152086)
NAKAMOTO Hiroshi Kawasaki Medical School, School of Medicine, Research Associate, 医学部, 助手 (10299183)
GOTO Masami Kawasaki College of Allied Health Professions, Medical Engineering, Professor, 臨床工学科, 教授 (50148699)
OGASAWARA Yasuo Kawasaki Medical School, School of Medicine, Associate Professor, 医学部, 助教授 (10152365)
KAJIYA Fumihiko Kawasaki College of Allied Health Professions, Medical Engineering, Professor (70029114)
|
|---|
| Project Period (FY) |
2004 – 2006
|
| Keywords | H_2O_2 / reactive hyperemia / mesenteric microcirculation / EDRF |
|---|
| Research Abstract |
We constructed the pencil-typed imaging system to evaluate the disturbance of mesenteric and coronary microcirculation during reactive hyperemia (RH). We have succeeded in quantitatively evaluating the in-vivo microcirculation with our videomicroscope system. Mesenteric arterioles from wild-type and Cu, Zn-SOD^<-/-> mice were continuously observed by a microscope during acetylcholine (ACh)-induced vasodilatation and RH in the cyclooxygenase blockade under the following 3 conditions; control, L-NMMA, and L-NMMA+catalase. In the mesenteric arterioles of wild-type mice, endothelium-dependent relaxations to ACh and vasodilatation during RH were resistant to L-NMMA, but were markedly inhibited by L-NMMA+catalase. In mesenteric arterioles of Cu, Zn-SOD^<-/->mice, L-NMMA markedly inhibited the relaxations to ACh and vasodilatation during RH but were not inhibited by the addition of catalase. RH-induced increase in blood flow after L-NMMA was significantly increased in the wild-type mice by microsphere, whereas in the Cu, Zn-SOD^<-/-> mice, it was significantly reduced. In the mesenteric arterioles of the Cu, Zn-SOD^<-/-> mice, tempol, an SOD mimetic, significantly increased the ACh-induced vasodilatation, and the enhancing effect of tempol was abolished by catalase. Endothelial Cu, Zn-SOD plays an important role for the endogenous H_2O_2 that contributes to RH in mouse mesenteric microvessels in vivo.
|
