Clinical adoptable brain ischemic tolerance induced by modified electroconvulsive shock
| Project/Area Number |
14571477
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Anesthesiology/Resuscitation studies
|
|---|
| Research Institution | Kurume University |
|---|
Principal Investigator |
MIYAGAWA Yoshikado Kurume University, School of medicine, Anesthesiology, Assistant, 医学部, 助手 (20312150)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HARADA Hideki Kurume University, School of medicine, Anesthesiology, Assistant Professor, 医学部, 講師 (30198923)
|
|---|
| Project Period (FY) |
2002 – 2004
|
| Project Status |
Completed (Fiscal Year 2004)
|
| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
|---|
| Keywords | Ischemic tolerance / electroconvulsive shock / rat forebrain ischemia / rat focal cerebral ischemia / rat spinal cord ischemia model / 電気痙攣療法 |
|---|
| Research Abstract |
Many investigators have demonstrated that minor stress such as sublethal ischemia, heat, and cortical spreading depression could make neurons more tolerant to subsequent lethal ischemic insults in animal model. Even though the concept of ischemic tolerance is crucial, all of these procedures are too invasive to be applied in clinical use. Previous animal studies have suggested that electroconvulsive shock(ECS) increases neuronal activities and then could cause rapid molecular responses of heat shock families, immediate early genes and trophic factors, which are involved to acquire neuronal ischemic tolerance. In this study we have tested in rats the hypothesis that ECS is an effective measure to acquire cross-tolerance against subsequent focal cerebral ischemia.
Materials and Methods : 43 Wistar male rats were randomly allocated to one of the following four groups. First group received repeated ECS once a day for 9 consecutive days (rECS). Second group received single ECS(sECS). Third g
… More
roup of untreated with ECS rats were served as control (Control). Fourth group, which received sECS or rECS without ischemic insult, was prepared as a sham group(Sham).
Every ECS(50mA,3.0s) was administered via ear-clip electrodes just before awakened from isoflurane-oxygen anesthesia. All animals treated with ECS showed a full tonic-clonic attack, followed by hind limb extension and stuporous phase. In rECS and sECS groups, ischemia was induced 2 days after the last ECS. The ischemic time was 45 minutes using intraluminal middle cerebral occlusion technique under awakeful status. 2 days after the ischemic insults, rats were sacrificed by decapitation, and the infarction volume was calculated in TTC stained coronal planes.
Results : Infarction volumes in the cortex and subcortex were significantly smaller in the sECS group (75.6+/-52.87 mm, and 53.69+/-18.98mm, respectively) than those in the control group (173.39+/-53.86 mm p=0.0012 and 72.28+/-11.34 mm, p=0.0223 respectively). The infarct volume of cortex in the rECS(112.4+/-47.86 mm, p=0.0305) group was also significantly smaller, compared with that in the control group, while the infarct area of subcortex (68.72+/-10.96 mm, p=0.6432) did not show significant reduction.
Conclusion : This data suggest that ECS at 48 hours before ischemia reduces the infarction volume subjected to lethal focal cerebral ischemia. ECS may have a possibility as a novel pretreatment for surgery in which temporary ischemia is unavoidable. Less
|
Report
(4 results)
Research Products
(5 results)
