EFFECTS OF HEXAMETHONIUM, BIPERIDEN AND PHENTOLAMINE ON VASOCONSTRICTIVE EFFECTS OF OCULOMOTOR NERVE-STIMULATION IN RABBITS
EFFECTS OF HEXAMETHONIUM, BIPERIDEN AND PHENTOLAMINE ON VASOCONSTRICTIVE EFFECTS OF OCULOMOTOR NERVE-STIMULATION IN RABBITS
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DOI：
10.1016/0014-4835(76)90220-7
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发表时间：
1976-01-01
影响因子：
3.4
通讯作者：
ALM, A
中科院分区：
文献类型：
--
作者：
BILL, A;STJERNSCHANTZ, J;ALM, A
家兔动眼神经颅内刺激引起葡萄膜前血管收缩和脉络膜血管扩张，并试图分析刺激引起血管收缩反应的机制。单侧刺激动眼神经，用放射性标记微球测定双眼局部血流量。剂量为40-80 mg/kg体重的六甲溴铵完全消除了虹膜和睫状体突的血管收缩反应。受刺激侧葡萄膜各部位的血流量往往高于对照组。在2.5- 5mg /kg体重剂量下，双叶草乳酸副交感神经溶解剂降低了虹膜的反应，但在睫状体突中未观察到明显变化。.alpha。-肾上腺素能阻滞剂氯酚妥拉明，剂量为10-15 mg/kg体重时，对虹膜的反应无显著影响，但对睫状体突的作用相反。双哌啶联合酚妥拉明完全消除了虹膜血管收缩反应，刺激侧睫状体的血流量增加。颅内刺激动眼神经和可能的邻近结构明显引起葡萄膜血管舒张剂和血管收缩剂的释放。血管收缩作用部分是毒蕈碱，可能是由于收缩，部分是由于刺激对酚妥拉明敏感的受体。在刺激点和效应细胞之间的某个地方，神经节或神经节样受体似乎参与了血管收缩冲动的传递。
In rabbits intracranial stimulation of the oculomotor nerve causes vasoconstriction in the anterior uvea and vasodilation in the choroid and an attempt was made to analyze the mechanism involved in the vasoconstrictive response to stimulation. The oculomotor nerve was stimulated unilaterally, and regional blood flow was determined in both eyes using radioactively labeled microspheres. Hexamethonium bromide, in a dose of 40-80 mg/kg body weight, completely abolished the vasoconstrictive response in the iris and the ciliary processes. The blood flow in all parts of the uvea tended to be higher on the stimulated side than on the control side. The parasympatholytic agent biperiden lactate, in a dose of 2.5-5 mg/kg body wt, reduced the response in the iris, but no significant change was observed in the ciliary processes. The .alpha.-adrenergic blocking agent phentolamine chloride, in a dose of 10-15 mg/kg body wt had no significant effect on the response in the iris but reversed the effect in the ciliary processes. A combination of biperiden and phentolamine totally abolished the vasoconstrictive response in the iris, and there was increased blood flow in the ciliary processes on the stimulated side. Intracranial stimulation of the oculomotor nerve and possibly of adjacent structures apparently caused a release of vasodilating and vasoconstricting agents in the uvea. The vasoconstrictive effect was partly muscarinic, possibly due to miosis, and partly due to stimulation of receptors sensitive to phentolamine. A ganglion or ganglion-like receptors, somewhere between the site of stimulation and the effector cells, seem to be involved in the transmission of the vasoconstrictive impulses.