1988 Fiscal Year Final Research Report Summary
Metabolical and morphological study for endothelial cell injry and platelet aggregation in childhood disorders.
| Project/Area Number |
62570432
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | Kumamoto University |
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Principal Investigator |
MIIKE Teruhisa Kumamoto University Medical School,Professor Department of Child Development., 医学部, 教授 (90040617)
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| Co-Investigator(Kenkyū-buntansha) |
KODAMA Mihoko Same as above, assistant, Department of Child Development, 医学部附属病院, 助手 (00178287)
NARUKAMI Hiroshi Kumamoto University Medical Hospital, Instructor, Department of Child Developmen, 医学部附属病院, 講師 (70040623)
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| Project Period (FY) |
1987 – 1988
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| Keywords | serotonin / endothelial cell injury / platelet aggregation / Duchenne muscular / dystrophy / dustrophin |
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| Research Abstract |
It has been reported that endothelial alterations including blister-like swelling, were observed in experimental serotonin myopathy as well as Duchenne muscular dystrophy (DMD).
In the first study, we observed blood vessels in rat muscle tissues after serotonin injection.
(1).Serotonin experiment. serotonin (75mg/Kg) was injected to Wister rats intraperitoneally. Althouge no structural damage was observed with the light microscope, ultrastructural changes were prominent in-muscle capillaries. One of the more impressive abnormalities consisted of large blister-like swelling, which appeared to originate from the luminal surface of the endothelial cell and extend into the lumen, at times almost completely occluding it. These phnomena were quite similar to those seen in DMD muscle tissue.
(2).Immunohistochemical study using antibodies against DMD gene product (dystrophin). Dystrophin was clearly localized in the surface membrane of smooth muscle layers (tunica media) of blood vessels of any kinds and sizes, especially muscular arteries, in various tissues from rats and mice. Ten hours after serotonin injection, bolld vesse in lung , even muscular arteries, lost dystrophin reaction. These results suggested that, dysfunction of tunica media, due to defective dystrophin and secondary damage by serotonin injection for instance, induce endothelial cell damage and platelet aggregation. On second thought, it wa suggested that, any conditions which induce platelet aggregation resulting abundant serotonin release in blood vessels, also produce endothelial cell injury.
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