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題名 | Effects of Naloxone on Cerebral Catecholamines and Electrolytes in Cerebral Ischemia Induced by Carotid Occlusion in Gerbils=Naloxone對腦缺血沙鼠之腦組織內兒茶胺及電解質的影響 |
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作者 | 顏茂雄; 吳錦楨; 邱文慧; | 書刊名 | 醫學研究 |
卷期 | 7:6 1987.05[民76.05] |
頁次 | 頁295-302 |
分類號 | 418.1 |
關鍵詞 | 內兒茶胺; 沙鼠; 組織; 腦; 腦缺血; 電解質; 影響; |
語文 | 英文(English) |
中文摘要 | 本研究目的有二:(一)觀察naloxone是否具改善腦缺血所引起的神經症狀?(二)探討改善腦缺血症狀之可能原因。本實驗是以單側頸動脈結紮沙鼠作為研究對象。結果顯示沙鼠經單側頸動脈結紮後六小時,從外觀上,可觀察到各種神經症狀,諸如:半身癱瘓,自發性繞圈動作,跳躍及癲癇發作等。上述的神經症狀可經由腹腔注射naloxone(3-5 mg/kg)而明顯改善。此外,缺血部位的腦組織,在結紮後六小時,含水量及納離子濃度增加,而鉀離子濃度減少,這說明了腦缺血後,會引起嚴重腦水腫現象,然而,naloxone對此腦水腫現象並無明顯的改善作用。此外,腦組織在六小時缺血情況下,正腎上腺素(NE)與多巴胺(DA)的濃度顯著降低,然而經naloxone治療後,此種現象可被減緩。由上述結果顯示naloxone其改善因腦缺血所引起的神經症狀,可能與中樞茶胺(catecholamines)的濃度有密切關係。 |
英文摘要 | The effects of naloxone on cerebral ischemia induced by unilateral carotid ligation were studied in Mongolian gerbils. The neurological deficits eg. hemiparesis, spontaneous circular movement, jump and seizure were recognized following unilateral carotid occlusion. These symptoms were significantly improved after treatment with naloxone (3-5 mg/kg, i.p.). Water and sodium content increased although potassium decreased following 6 hrs. of carotid ligation. This indicated that the cerebral edema was formed after 6 hrs. of ischemia. However, the change of water, Na+ and K+ did not indicate a statistically difference between the naloxone and untreated groups. On the other hand, norepinephrine (NE) and dopamine (DA) levels in the ischemic area were significantly decreased after 6 hrs. of carotid ligation in comparison with the sham-operated animals. Furthermore, this reduction of monoamine level in carotid ligation of untreated groups was significantly attenuated by the treatment of naloxone. In conclusion, the results demonstrated that the neurological deficits, catecholamine reduction and an increase in water and sodium were observed in cerebral ischemia. Naloxone had a significant improvement on neurological deficit and attenuated catecholamine reduction. However, there was no significant effect on water and electrolyte changes in the tissues of cerebral ischemia. This implied that the possible mechanism of naloxone, in improving neurological deficits caused by cerebral ischemia, may relate to alteration of monoamine level in the ischemicarea. |
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