Pharmacological effects of pilocarpine on rabbit ciliary artery
Pharmacological effects of pilocarpine on rabbit ciliary artery
复制标题
毛果芸香碱对兔睫状动脉的药理作用
DOI：
10.1076/0271-3683(200004)2041-5ft254
复制
发表时间：
2000
影响因子：
2
通讯作者：
E. Hayashi
中科院分区：
文献类型：
--
作者：
T. Yoshitomi;H. Ishikawa;E. Hayashi
目的.眼血流障碍是青光眼引起的视觉损害的发病机制中的重要因素。我们研究了睫状动脉的神经支配，重要的血流在视神经乳头，和毛果芸香碱的影响。方法.从兔眼制备睫状动脉，并安装在肌描记系统中。用等长张力记录法观察了神经电刺激和毛果芸香碱对离体兔睫状动脉的作用。结果电场刺激诱发睫状动脉收缩，10 µM布那唑嗪预处理可抑制睫状动脉收缩。在存在或不存在内皮的情况下，当睫状动脉被10 μM组胺预收缩时，电场刺激也引起舒张。用10 µM N-硝基-L-精氨酸甲酯（L-NAME）预处理可抑制这种舒张。毛果芸香碱给药产生剂量依赖性肌肉松弛，L-NAME、1 µM阿托品或内皮剥脱可消除这种松弛。结论.结果表明，兔睫状动脉的神经支配至少有两种不同类型的神经，肾上腺素能神经，引起收缩和神经纤维，导致内皮非依赖性释放一氧化氮（NO）。毛果芸香碱松弛这肌肉依赖于内皮细胞和NO的合成。
Purpose. A disturbance in ocular blood flow is an important factor in the pathogenesis of visual damage caused by glaucoma. We investigated the innervation of the ciliary artery, important to blood flow in the optic nerve head, and the effects of pilocarpine thereon. Methods. Ciliary arteries were prepared from rabbit eyes and mounted in a myograph system. The effects of electrical nerve stimulation and pilocarpine on the isolated rabbit ciliary artery were investigated using isometric tension recording methods. Results. Electrical field stimulation evoked contraction of the ciliary artery, which was inhibited by pretreatment with 10 µM bunazosin. Electrical field stimulation also evoked relaxation when the ciliary artery was pre-contracted by 10 µM histamine in the presence or absence of endothelium. This relaxation was inhibited by pretreatment with 10 µM N G -nitro-L-arginine methylester (L-NAME). Pilocarpine administration produced a dose-dependent muscle relaxation that was abolished by treatment with L-NAME, 1 µM atropine, or denudation of the endothelium. Conclusions. Results indicate that the rabbit ciliary artery is innervated by at least two different types of nerves, adrenergic nerves, which evoke contraction and nerve fibers that cause an endothelium-independent release of nitric oxide (NO). Pilocarpine relaxation of this muscle was dependent on the endothelium and NO synthesis.