The septic shock-induced decrease in mesenteric blood flow and release of proinflammatory cytokines are among the major pathophysiologic changes presumed to lead to multiple organ dysfunction syndrome (MODS). Increased nitric oxide (NO) levels are associated with both decreased mesenteric blood flow and positive modulation of proinflammatory cytokine release. In this study we aimed to determine the effect of the timing of the inhibition of nitric oxide synthase (NOS) on mesenteric blood flow and serum interleukin-10 (IL-10) concentrations during endotoxin shock. A nonspecific NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME), a specific NOS inhibitor aminoguanidine (AG), or placebo were injected 20 minutes before or 20 minutes after a lipopolysaccharide (LPS) or placebo challenge to Swiss-albino mice, as pretreatment or posttreatment, respectively. At 120 minutes after LPS or placebo injection the mesenteric blood flow was measured, and blood samples from the heart were obtained for IL-10 levels in both groups. Pretreatment and posttreatment with both NOS inhibitors prevented the LPS-induced decrease in mesenteric blood flow. Pretreatment was more effective for this purpose. Pretreatment accentuated the LPS-induced increase in serum IL-10 concentrations, whereas posttreatment had no significant effect. We conclude that the timing of NOS inhibition is important for attenuating some deleterious effects of endotoxin.

译文

:败血性休克引起的肠系膜血流量减少和促炎性细胞因子释放是导致多器官功能障碍综合症(MODS)的主要病理生理变化之一。一氧化氮(NO)水平升高与肠系膜血流量减少和促炎性细胞因子释放的正调节有关。在这项研究中,我们旨在确定内毒素休克期间一氧化氮合酶(NOS)抑制时机对肠系膜血流和血清白介素10(IL-10)浓度的影响。在脂多糖(LPS)或安慰剂攻击Swiss-20之前或之后20分钟注射非特异性NOS抑制剂NG-硝基-L-精氨酸甲酯(L-NAME),特异性NOS抑制剂氨基胍(AG)或安慰剂。白化病小鼠,分别作为预处理或后处理。在LPS或安慰剂注射后120分钟,测量肠系膜的血流,并从两组的心脏中获取血样中的IL-10水平。两种NOS抑制剂的预处理和后处理均防止了LPS诱导的肠系膜血流量的减少。为此目的,预处理更为有效。预处理加重了LPS诱导的血清IL-10浓度的增加,而后处理则无明显影响。我们得出结论,抑制NOS的时机对于减弱内毒素的某些有害作用很重要。

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