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本实验用ＮＡＤＰＨ－黄递酶（ＮＤＰ）组织化学染色法观察了自发性高血压大鼠（ＳＨＲ）和京都种大鼠（ＷＫＹ，正常对照）视网膜内一氧化氮合酶（ＮＯＳ）的变化。结果显示，ＮＯＳ阳性神经元位于内核层和视网膜节细胞层。ＳＨＲ组视网膜ＮＯＳ阳性细胞属无长突细胞和移位无长突细胞。偶见阳性的节细胞。ＮＯＳ阳性无长突细胞和节细胞胞质显强阳性反应，可见较长而清晰的突起。ＮＯＳ阳性神经元的分布密度大，且在视网膜中央区（视神经盘附近）的分布密度略大于周围区。在ＷＫＹ正常对照组，ＮＯＳ阳性无长突细胞和节细胞的反应不如ＳＨＲ组强，突起较短且纤细。ＮＯＳ阳性细胞的分布密度低于ＳＨＲ组。自发性高血压大鼠视网膜无长突细胞内一氧化氮合酶表达增加，提示一氧化氮在视网膜缺氧缺血的情况下，可能参与神经细胞损伤的过程，具有神经毒性。
In this study, the changes of nitric oxide synthase (NOS) in the retina of spontaneously hypertensive rats (SHR) and Kyoto rats (WKY, normal control) were observed by NADPH-diaphorase (NDP) histochemical staining. The results showed that NOS positive neurons were located in the inner nuclear layer and the retinal ganglion cell layer. Retinal NOS positive cells in SHR group were amacrine cells and translocated amacrine cells. Occasionally positive cells of the joints. NOS-positive amacrine cells and cytoplasm cells were significantly positive reaction, showing a longer and clear protrusions. NOS positive neurons are densely distributed and slightly more densely distributed in the central retinal area (near the optic disc) than in the peripheral area. In WKY normal control group, the reaction of NOS positive amacrine cells and ganglion cells was not as strong as that of SHR group, and the protrusions were shorter and slender. The distribution density of NOS positive cells was lower than that of SHR group. Spontaneous hypertensive rats retinal amastigotes nitric oxide synthase expression increased, suggesting that nitric oxide in the retina hypoxic-ischemic situation may be involved in the process of nerve cell injury, with neurotoxicity.