Effects of Lipoxygenase Inhibitor on Cerebral Edema Induced by Freezing Lesion in Rats

脂氧化酶抑制劑對冷凍引起腦水腫之影響

顏茂雄(Mao-Hsiung Yen) ； 李素華(Swu-Hua Lee)

《The Chinese Journal of Physiology》 33卷4期 (1990/12) Pp. 385-397

摘要

本實驗目的擬利用NDGA，一種脂氧化酶(lipoxygenase)抑制劑對腦水腫之影響，以進一步瞭解花生四烯酸(arachidonic acid)代謝物在腦水腫致病因中所扮演角色。本實驗腦水腫模式是以冷凍大腦皮質所引起。實驗結果顯示，受傷部位及其附近組織對Evans blue之通透性明顯增加。上述現象於受傷後24小時達最顯著。此外，腦內壓由假性組的5.6±0.4 mmHg增加至受傷組的11.1±0.8 mmHg，而受傷部位與對側未受傷部位腦組織之含水量，則分別為82.7±0.4％與79.9±0.3％；同時受傷部位組織之納、鈣等離子濃度明顯增加，相反的鉀濃度則減低。至於24小時腦水腫動物經NDGA（3 mg/kg及6 mg/kg I.P.）48小時前預處理時，則此腦內壓、組織含水量及納、鉀等逐漸恢復正常，至於鈣雖明顯降低但未恢復正常。此外，未經治療組與立即給藥組間則無明顯差異。由本實驗結果證明NDGA確實具有改善腦水腫之作用，因而初步認為花生四烯酸代謝物可能為引起腦水腫致病因之重要因素之一。

並列摘要

Yen, M.H., and S.H. Lee. Effects of lipoxygenase inhibitor on cerebral edema induced by freezing lesion in rats. Chinese J. Physiol. 33(4): 385-397, 1990. This study was done to examine the effect of the lipoxygenase inhibitor, nordihydroguaiaretic acid(NDGA), on cerebral edema and to substantiate the hypothesis that the metabolites of arachidonic acid are involved in the pathogenesis of cerebral edema. The experiment was performed on rats with vasogenic cerebral edema induced by a freezing lesion. Results demonstrate that the permeability of blood-brain barrier to macromolecules, assessed by Evans blue, was progressively increased and reached a maximum at 24 hrs after freezing untreated rats. At 24 hrs following cold injury, the intracranial pressure was significantly increased from 5.6±0.4 mmHg to 11.1±0.8 mmHg and water content from 79.9±0.3% to82.7±0.4%. Sodium and calcium contents increased but potassium decreased significantly as found in untreated cerebral edema tissues. In the nordihydroguaiaretic acid pretreatment group, (3 mg/kg & 6 mg/kg, i.p., 48 hrs in advance)intracranial pressure, water, sodium, and calcium contents were significantly decreased but potassium was increased in cerebral edema tissues. There was no significant difference between untreated controls and immediately post-treated animals. Since NDGA substantially alleviated brain edema, the results suggest that the metabolites of arachidonic acid resulting from the lipoxygenase pathway may contribute to the pathogenesis of cerebral edema.

並列關鍵字

lipoxygenase inhibitor ； nordihydroguaiaretic acid ； cerebral edema