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作 者:梁福波[1] 陈家津[1] 陈文芳[1] 陈蕾[1]
机构地区:[1]青岛大学医学院生理教研室
出 处:《动物学报》1997年第4期361-365,共5页ACTA ZOOLOGICA SINICA
摘 要:注射微量β内啡肽入Wistar大鼠侧脑室,探讨其对血浆唾液酸水平的影响及其可能机制。结果表明:(1)侧脑室注射β内啡肽后,血浆唾液酸水平较对照组明显降低(P<001),而且唾液酸水平降低的时间随β内啡肽浓度的增加而逐渐缩短;(2)静脉注射酚托拉明后,侧脑室注射β内啡肽,血浆唾液酸水平明显降低(P<001);(3)静脉注射心复宁后,侧脑室注射β内啡肽,血浆唾液酸水平明显降低(P<001);(4)静脉注射阿托品后,侧脑室注射β内啡肽,血浆唾液酸水平无明显变化(P>005)。这提示外源性的β内啡肽参与了降低大鼠血浆唾液酸水平的调节过程,其机制系与乙酰胆碱的释放经胆碱能m型受体起作用密切相关,并可能通过副交感神经实现此效应。Experiments were performed on 48 healthy male Wistar rats Weighing 180~220g. The methods involved microinjection into the lateral ventricle (LV) and spectrophotometry to study the effect of β Endorphin (β END) on plasma sialic acid (SA) level and the possible mechanism. The results indicate: (1) The plasma SA level was significantly decreased after the micro injection of β END into LV (P<0.01) and the time required to cause the decrease was shortened with the increase of β END concentration; (2) The plasma SA level decreased significantly after β END microinjection which followed the intravenous injection of Phentolamine or Pindolol (P<001); (3) The plasma SA level remained unchanged after the microinjection of β END which followed the intravenous injection of Atropine (P>005). These results suggest that the possible mechanism by which β END causes the decrease of plasma SA level is related to the release of Ach and through the cholinergic muscarinic receptor.
分 类 号:R335[医药卫生—人体生理学] Q959.837[医药卫生—基础医学]
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