摘要
目的:从神经-受体-受体介导睫状肌细胞内反应角度探讨肝劳发生的机制。方法:选用与猿猴解剖特点极其接近的动物树鼠句,对其限定照明时间并予以形觉刺激诱视,造成树鼠句持续近视状态以模拟肝劳的病理变化。在实验的第3,6,9天分别处死模型组及正常对照组动物,取睫状体检测其中β-肾上腺素受体(β-AR),环磷酸腺苷(cAMP),环磷酸鸟苷(cGMP)和Na+-K+-ATP酶;以确定造模3,6,9d3个不同时段对动物的影响。结果:造模6d时,树鼠句睫状肌中β-AR发生了上行调节;造模6d时,β-AR睫状肌中cAMP含量显著升高,cGMP含量降低;造模6d时,β-AR睫状肌中Na+-K+-ATP酶活力升高。结论:持续近视状态下睫状肌双重神经支配的异常为肝劳发病的重要原因之一。
AIM:To explore the initial function of asthenopia by analyzing nerve receptor change and receptor induced reaction inside ciliary muscle cell. METHODS:Tree shrews, which have similar anatomic features to the monkey, were used and induced to watch in limited illuminating periods. It could imitate pathological changes of asthenopia due to sustaining near sight status. After 3,6,9 days separately, animals in model group and controlled group were killed and their ciliary bodies were collected to estimate the beta AR,cAMP,cGMP and Na+ K+ ATP enzyme.Thus,the influence at three different intervals of 3, 6, 9 days was confirmed. RESULTS:Six days after model establishment,beta AR in ciliary muscle of tree shrew was moderately increased; camp in beta AR ciliary muscle was significantly higher, with the decrease of cGMP; Na+ K+ ATP enzyme activity enhanced. CONCLUSION:Disorder of ciliaris double innervation in the state of near sight is an important reason for asthenopia occurrence.
出处
《中国临床康复》
CSCD
2004年第17期3316-3318,共3页
Chinese Journal of Clinical Rehabilitation