After administration of L-N〓-nitro-Arginine, a specific antagonist of NOS, it was found that the basal and stimulated NO release of blood vessels (aorta, internal carotid, renal and mensenteric artery) was decreased further. The increase of coronary blood flow stimulated by Ach was also reduced further, while the platelet aggregation degree and erythrocyte aggregation index increased significantly. Pathological examination indicated that aortic endothelium was destroyed, the blood vessels in cerebral, cardiac and renal tissues were hypertrophied further and some were almost occluded. The above fin dings resulted in SHR feeded with L-NNA having high incidence of stroke rate and high degree of renal cirrhosis when compared to control SHR. The infarct and hemorrhagic focuci in cerebral tissues, infarct focuci in cardiac tissues, atrophy and hyalinedegeneration of renal glomeruli and degeneration even necrosis of renal tubuli in renal tissues were al so found. The increase ratio of brain and heart to body weight and decrease ratio of kidney to body wei ght further demonstrated that the cerebral, cardiac and renal injuries were aggravated.
在上述结果的基础上进一步给予SHR NOS特异性拮抗剂左旋亚硝基精氨酸后，血管(胸主、颈内、肾及肠系膜动脉)NO基础释放及激动剂刺激释放进一步减少，Ach刺激冠脉流量的增加和胸主动脉内膜NOS活性也进一步减少，血小板聚集程度及红细胞聚集指数显著上升，病理切片显示胸主动脉内皮细胞破坏明显，脑心肾组织内的血管进一步增厚甚至几乎阻塞，导致饲L-NNA的SHR缺血性及出血性脑卒中发生率显著高于对照SHR，脑体重比显著升高；心肌内出现明显的缺血梗塞疤痕灶，心体重比显著升高；肾小球明显萎缩、玻璃样变性，肾小管也变性甚至坏死，使肾硬化程度显著增加呈颗粒性固缩肾，肾体重比也显著减少。