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首页> 外文期刊>Cytokine >Effects of a peripheral cholinesterase inhibitor on cytokine production and autonomic nervous activity in a rat model of sepsis
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Effects of a peripheral cholinesterase inhibitor on cytokine production and autonomic nervous activity in a rat model of sepsis

机译：外周胆碱酯酶抑制剂对脓毒症大鼠模型细胞因子产生和自主神经活动的影响

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Purpose: Recently, cholinergic anti-inflammatory pathway manipulation has been proposed as a new strategy to control cytokine production in sepsis. We investigated whether hypercytokinemia can be controlled via this pathway in an animal model of sepsis, with concomitant monitoring of autonomic nervous activity involving heart rate variability (HRV) analysis of electrocardiographic R-R intervals. Methods: Sixty-eight adult male Sprague-Dawley rats were used (28 for examination of cytokine production and autonomic nervous activity; 40 for survival analysis). Each part of the study involved four animal groups, including two control groups without drug administration. Sepsis was induced by cecal ligation and puncture (CLP). Distigmine bromide, a peripheral, non-selective cholinesterase inhibitor (0.01. mg/kg), was administered subcutaneously 90. min after surgery. Continuous electrocardiograms were recorded for 5. min before and after surgery (at intervals of 5. h) in CLP and sham-operated animals for HRV analysis. Blood samples were collected 20. h after surgery for serum cytokine and catecholamine assay. Results: On HRV analysis, distigmine inhibited reduction of total power and high-frequency components in CLP animals (P<0.05). Distigmine significantly inhibited cytokine induction (IL-6 and IL-10) (P<0.01) as well as increase in serum levels of noradrenaline and dopamine (P<0.05). Distigmine did not significantly improve CLP animal survival rate. Conclusions: The cholinesterase inhibitor distigmine inhibited induction of inflammatory cytokines and catecholamines as well as HRV suppression in a rat CLP model, suggesting that an agent modulating the cholinergic anti-inflammatory pathway can control excess cytokine production involved in the pathogenesis of severe sepsis/septic shock.
机译：目的：最近，胆碱能抗炎途径的操作已被提议作为控制败血症中细胞因子产生的新策略。我们调查了败血症动物模型中是否可以通过此途径控制高细胞血症，并伴随监测包括心电图R-R间隔的心率变异性（HRV）在内的自主神经活动。方法：使用68只成年雄性Sprague-Dawley大鼠（28只用于检查细胞因子的产生和自主神经活动; 40只用于存活分析）。研究的每个部分都涉及四个动物组，其中包括两个不使用药物的对照组。盲肠结扎和穿刺（CLP）引起败血症。手术后90分钟皮下注射溴化二甲胺，一种外周性非选择性胆碱酯酶抑制剂（0.01。mg / kg）。在CLP和假手术动物中，在手术前后（以5小时为间隔）记录连续5分钟的连续心电图，以进行HRV分析。手术后20小时收集血样用于血清细胞因子和儿茶酚胺测定。结果：在HRV分析中，二甲胺抑制了CLP动物的总功率和高频成分的降低（P <0.05）。 Distigmine显着抑制细胞因子的诱导（IL-6和IL-10）（P <0.01）以及去甲肾上腺素和多巴胺的血清水平升高（P <0.05）。 Distigmine不能显着提高CLP动物的存活率。结论：胆碱酯酶抑制剂二甲双胍抑制大鼠CLP模型中炎性细胞因子和儿茶酚胺的诱导以及HRV抑制，表明调节胆碱能抗炎途径的药物可以控制严重脓毒症/脓毒性休克的发病机理中涉及的细胞因子产生。 。

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