日本医科大学雑誌
Online ISSN : 1884-0108
Print ISSN : 0048-0444
ISSN-L : 0048-0444
虚血性脳浮腫におけるfree radicalの影響
稲村 憲治
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ジャーナル フリー

1982 年 49 巻 5 号 p. 618-626

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抄録
The hypothesis that “Free radical reaction” plays a role in production of ischemic brain edema was checked in the ischemic model produced in the Mongolian gerbil through unilateral carotid ligation (ULCL). Free radical is a highly reactive state of molecule with a single electron at the most outer orbit. By its highly reactive nature, free radical affects the lipid bilayer membrane to produce lipid peroxides it also affects enzyme activities. As an index of free radical activity, the author periodically measured cerebral tissue lipid peroxide level. As an index of cytologic membrane damage, the author measured cerebral tissue acid phosphatase activity. Water content and passage of 18I-RISA were also periodically measured.
In the animals which showed neurological symptoms following ULCL, water content began to rise after 2 to 3 hours after ULCL, reaching its peak at 18 to 48 hours. There was no rise of water content on the contralateral hemisphere.
The 181I-RISA uptake rose only after 12 hours following ULCL only on the ipsilateral hemisphere. This may indicate that the blood brain barrier was still intact till 12 hours after ULCL. The tissue lipid peroxide level rose after ULCL and reached its peak 6 hours after ULCL on the damaged hemisphere. This fact may indicate that free radical reaction was active during this period while the blood brain barrier was still intact.
The total phosphatase activity showed little alteration, but the free acid phosphatase activity of the damaged hemisphere showed elevation at 6 to 24 hours after ULCL. This fact may indicate that the membrane damage had occurred during this period. Since acid phosphatase is usually confined to lysosomes and other membrane particles, the release of the enzyme may be due to the membrane damage.
These results suggest that during the early phase of ischemic brain edema, lipid peroxidation of the membrane occurs as a result of free radical activity. This membrane damage involves plasma membranes as well as membranes of blood brain barrier, thereby enhancing brain edema.
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