论文部分内容阅读
阐明在尼古丁所引起的家犬视网膜动脉舒张反应中所包含的神经源性一氧化氮（ＮＯ）作用机制．利用离体除去内皮细胞的家犬视网膜动脉标本，观察其张力改变．尼古丁引起前列腺素Ｆ２预收缩的家犬视网膜动脉舒张反应，其舒张反应被六甲铵和氧合血红蛋白所消除，但不受吲哚美辛，阿托品及塞吗洛尔的影响．ＮＯ合酶抑制剂左旋硝基精氨酸（Ｌ－ＮＡ）可消除尼古丁所致舒张反应并使其舒张转为收缩反应，而右旋硝基精氨酸无此作用．Ｌ－ＮＡ所致此抑制作用可被ＮＯ合成前体左旋精氨酸所复原，而不受右旋精氨酸的影响．本研究表明家犬视网膜动脉上存在舒张血管神经，该神经通过释放ＮＯ神经递质引起该血管舒张反应．
To elucidate the mechanism of neuronal nitric oxide (NO) involved in nicotine-induced retinal artery vasorelaxation in dogs. Retinal arterial samples of domestic dogs were removed by endothelial cells and the changes of tension were observed. Nicotine causes the retinal artery vasorelaxation in dogs pre-contracted with prostaglandin F2, and its vasodilatory response is abolished by hexamethonium and oxyhemoglobin but is not affected by indomethacin, atropine, and sevomibal. L-NA, a NO synthase inhibitor, abolished nicotine-induced relaxation and diastolic into a contractile response, whereas dextrorotatory arginine did not. This inhibition by L-NA can be restored by L-arginine, an NO-synthesizing precursor, independent of L-arginine. This study shows that there are diastolic vascular nerves in the canine retina arteries, which cause this vasodilation by releasing NO neurotransmitters.