| Project/Area Number |
08671764
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Anesthesiology/Resuscitation studies
|
|---|
| Research Institution | WAKAYAMA MEDICAL COLLEGE |
|---|
Principal Investigator |
IRANAMI Hiroshi Wakayama Medical College Medicine Associate Profesor, 医学部, 講師 (30193692)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HATANO Yoshio Wakayama Medical College Medicine Professor and Chair, 医学部, 教授 (70115913)
|
|---|
| Project Period (FY) |
1996 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
|
| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
|
|---|
| Keywords | nitric oxide / volatile anesthetics / vascular dilation / phospholipase / G protein / 揮発性麻酔薬 / 血管弛緩反応 |
|---|
| Research Abstract |
The current study was aimed to clarify the signal transduction mediating the phospholipase A2- stimulated EDRF production which is one of the major mechanism underlying endothelial vascular tone control via basally released EDRF and to examine the effects of volatile anesthetics on the vascular dilation phenomen.
The results of the current study indicated that (1) activated phospholipase A2 directly by melittin or indirectly by A1F and vanadate mediated EDRF release from endothelium by means of endothelial Ca2+/Calmoduline-independent nitric oxide synthase, in which arachidonate metabolites by lypoxygenase and cytochrome P450 played possible crucial roles, (2) halothane but not isotlurane or sevoflurane inhibited this relaxation mechanism stimulated by direct activation of phospholipase A2 with mellitin and (3) no anesthetics inhibited this relaxation mechanism stimulated by indirect activation of phospholipase A2 with G protein activators, A1F and vanadate.
Accordingly, the current study showed the novel signal prunsduction mediating endothelial phospholipase A2-induced EDRF production and inhibitory action of halothane, unlike other anesthetics, on this mechanism . The findings in the current study will be substituted to the pharmacological papers.
|
