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目的按照经典理论．在败血症休克（ＳＳ）发病机理中，交感神经，儿茶酚胺（ＣＡ）起主导作用，此理论沿用至今，但它与临床实践有明显矛盾并难以指导临床、为此，我们将ＣＡ均有明显增高而临床症状截然相反的ＳＳ与神经源性肺水肿（ＮＥＰ）进行部分病理生理比较研究，以期从两者差别及ＳＳ的特殊性中，揭示其发病机理。此文为实验一部分。方法肺系数、ＣＡＰ、ＰＡＰ、ＣＡＷＰ、微循环观察、血浆ＥＴ－１，ＮＯ测定；ＳＳ时ｉＮＯＳｍＲＮＡ肺组织原位杂交、ｎｏｒｔｈｅｒｎ ｂｌｏｔ、原址ＰＣＲ；胞内 Ｃａ＋＋，胞内１Ｐ１、１Ｐ２、１Ｐ３测定。结果部分生理学指标显示；交感，ＣＡ占优势的不是ＳＳ而是ＮＰＥ。 ＮＰＥ时血管病理性收缩，ＥＴ－增高明显；而ＳＳ时血管有病理性扩张，ＮＯ增高明显，内皮细胞内 Ｃａ＋＋，ＩＰ３增高，肺组织 ｉＮＯＳ ｍＲＮＡ表达增强；而 Ａｃｈ Ｍ受体抑制剂６５４－２能使上述状态减轻或消失，恢复正常状态。讨论根据以上实验结果及长期临床实践基础上，我们提出初步工作假说：在ＳＳ发病机理中，交感，副交感系统高水平失平衡基础上，以ＡＣｈ、ＮＯ为主导，ＮＯ与超氧阴离子结合成ＯＮＯＯ，继而形成·ＯＨ＋ＮＯ－２，对细胞产生强烈毒性，导致血管病理?
The purpose of the classic theory. In the pathogenesis of septic shock (SS), the sympathetic nerve, catecholamine (CA) plays a leading role, the theory used so far, but it has obvious contradictions with clinical practice and difficult to guide the clinical, for which we have significantly increased CA The clinical symptoms of opposite SS and neurogenic pulmonary edema (NEP) part of the pathophysiology comparative study, with a view to the difference between the two and the specificity of SS to reveal its pathogenesis. This article is part of the experiment. Methods Pulmonary coefficient, CAP, PAP, CAWP, microcirculation, plasma ET-1 and NO were measured. In situ hybridization of iNOS mRNA in lung tissue was performed by SSR, northern blot and in situ PCR. Intracellular Ca ++, intracellular 1P1, 1P2 and 1P3 were detected. The results of some physiological indicators show; sympathetic, CA dominant is not SS but NPE. Pathological NP-induced vasoconstriction and ET-elevation were significantly increased. In SS, blood vessels were pathologically dilated and NO increased significantly. Intracellular Ca ++ and IP3 were increased and iNOS mRNA expression was increased in lung tissue. However, Ach M receptor inhibitor 654-2 Can make the above state to reduce or disappear, return to normal state. Discussion Based on the above experimental results and long-term clinical practice, based on the preliminary work hypothesis we put forward: SS pathogenesis, sympathetic, parasympathetic system based on the high level of imbalance, with ACh, NO as the leading, NO and superoxide anion combined ONOO , Followed by the formation of · OH + NO-2, the cells have a strong toxicity, leading to vascular pathology?