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本工作观察了大鼠止血带休克、败血症休克和小肠缺血再灌注休克一氧化氮样舒张因子(NO-LRF)的变化及作用。结果表明,休克动物离体主动脉对去甲肾上腺素的反应降低,组织cGMP含量增加。NO合成前体L-精氨酸(L-Arg)或NO合成阻断剂L-硝基精氨酸(L-NNA)、可溶性鸟苷酸环化酶抑制剂亚甲基蓝(MB)分别增强或减弱休克动物主动脉的上述变化,且这些药物的作用不依赖于血管内皮的存在,提示休克时非内皮源的NO-LRF生成增多是血管对收缩物质反应性降低的原因之一。整体实验发现,L-NNA加重晚期休克动物的低血压并恶化预后,而L-Arg延缓休克动物的血压降低,减轻组织损伤,提示NO-LRF对机体有重要的保护作用,休克时非内皮源NO-LRF生成增多可能是机体的适应性代偿反应。
In this study, we observed the changes and effects of NO-LRF in tourniquet-induced shock, septic shock and intestinal ischemia-reperfusion injury in rats. The results showed that the response of isolated aorta to norepinephrine decreased and the content of cGMP increased in shocked animals. L-arginine (L-Arg), an inhibitor of NO synthesis, L-arginine (L-NNA) and methylene blue (MB), a synthetic guanidate cyclase inhibitor, increased or decreased, respectively Shock animal aorta changes, and the role of these drugs does not depend on the existence of the vascular endothelium, suggesting that non-endothelium source of NO-LRF generation increased blood vessels to reduce the reactivity of contractile substances one of the reasons. The whole experiment found that L-NNA aggravates the hypotension and aggravates the prognosis of late-shock animals, while L-Arg delays the blood pressure of shocked animals and reduces tissue damage, suggesting that NO-LRF has an important protective effect on the body. Increased production of NO-LRF may be the body’s adaptive compensatory response.