1991 Fiscal Year Final Research Report Summary
A Study of fat Embolism Syndrome
| Project/Area Number |
63570698
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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 |
Orthopaedic surgery
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| Research Institution | Mie University |
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Principal Investigator |
SHIOKAWA Yasuo Mie University Hospital Assistant Professor, 医学部附属病院, 講師 (80115708)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Takashi Mie University School of Medicine Junior Staff, 医学部, 助手 (70230399)
YOMOYA Hiroshi Mie University School of Medicine Junior Staff, 医学部, 助手 (30220776)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Fat Embolism Syndrome / Arachidonic Acid Cascade |
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| Research Abstract |
In 1988, fractions of the fatty acids such as subcutaneous fat, bone marrow fat and blood lipid in adult dogs were measured by preparatory experiment, and fractions of the fatty acids in pulmonary tissues in both fracture and non-fracture groups were also measured From the results, arachidonic acid revealed significantly higher level in the fracture group than that in non-fracture group. Moreover, developemnt of the fatty thrombosis in pulmonary tissues in the fracture group was identified by fatty staining.
Based on the above-mentioned experimental results, identification experiment of the hypothesis that arachidonic acid cascade may be related to the development of the fatty thrombosis was carried out from 1989 to 1990. Namely, Metabolites of the arachidonic acid (prostaglanding-E_2 [PGE_2], thromboxane-B_2 [TXB_2, 6-keto-prostaglandin-F_1 alpha [6-keto-PGF_1 alpha] and phospholipase-A_2 [PLA_2] being a rate-determining step of the arachidonic acid in the blood of the fracture group were chronologically measured, and PGE_2, TXB_2 and 6-keto-PGF_1 alpha extracted from pulmonary tissues in the fracture and non-fracture groups were also measured. From the results, no significant change was observed in these parameters in the blood, while PGE_2 and TXB_2 measured in the tissue extracts revealed significaly higher level in the fracture group than that in non-fracture group. As a function of the metabolite of the arachidonic acid pulmonary tissues, it was considered that arachidonic acid increases the thrombotic fat in pulmonary tissues because TXB_2 and PGE_2 elevate the pulmonary vascular contraction and agglutinant effect of the platelet.
The systemic model in not only fatty thrombosis only in the pulmonary tissue, but also in the fatty thrombosis syndrome being clinically observed, namely model being measurable the change of parameters in the blood should be discussed in the future.
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