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首页> 外文期刊>American Journal of Physiology >Endotoxin depresses heart rate variability in mice: cytokine and steroid effects.
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Endotoxin depresses heart rate variability in mice: cytokine and steroid effects.

机译：内毒素可降低小鼠的心率变异性：细胞因子和类固醇的作用。

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摘要

Heart rate variability (HRV) falls in humans with sepsis, but the mechanism is not well understood. We utilized a mouse model of endotoxemia to test the hypothesis that cytokines play a role in abnormal HRV during sepsis. Adult male C57BL/6 mice underwent surgical implantation of probes to continuously monitor electrocardiogram and temperature or blood pressure via radiotelemetry. Administration of high-dose LPS (Escherichia coli LPS, 10 mg/kg, n = 10) caused a biphasic response characterized by an early decrease in temperature and heart rate at 1 h in some mice, followed by a prolonged period of depressed HRV in all mice. Further studies showed that LPS doses as low as 0.01 mg/kg evoked a significant decrease in HRV. With high-dose LPS, the initial drops in temperature and HR were temporally correlated with peak expression of TNFalpha 1 h post-LPS, whereas maximal depression in HRV coincided with peak levels of multiple other cytokines 3-9 h post-LPS. Neither hypotension nor hypothermia explained the HRV response. Pretreatment with dexamethasone prior to LPS significantly blunted expression of 7 of the 10 cytokines studied and shortened the duration of depressed HRV by about half. Interestingly, dexamethasone treatment alone caused a dramatic increase in both low- and high-frequency HRV. Administration of recombinant TNFalpha caused a biphasic response in HR and HRV similar to that caused by LPS. Understanding the role of cytokines in abnormal HRV during sepsis could lead to improved strategies for detecting life-threatening nosocomial infections in intensive care unit patients.
机译：患有败血症的人的心率变异性（HRV）下降，但其机制尚不清楚。我们利用内毒素血症的小鼠模型测试了在败血症期间细胞因子在异常HRV中起作用的假设。成年雄性C57BL / 6小鼠接受外科手术探针植入，以通过无线电遥测法连续监测心电图，温度或血压。高剂量LPS​​（大肠杆菌LPS，10 mg / kg，n = 10）的给药引起了双相反应，其特征是某些小鼠在1 h时温度和心率较早降低，随后长时间的HRV降低所有的老鼠。进一步的研究表明，低至0.01 mg / kg的LPS剂量引起HRV的显着降低。使用大剂量LPS​​时，温度和HR的初始下降在时间上与LPS后1小时TNFalpha的峰值表达相关，而HRV的最大降低与在LPS后3-9小时的多种其他细胞因子的峰值水平相符。低血压和体温过低均不能解释HRV反应。在LPS之前用地塞米松进行的预处理显着减弱了所研究的10种细胞因子中的7种的表达，并使HRV抑制的持续时间缩短了约一半。有趣的是，单独的地塞米松治疗引起低频和高频HRV的急剧增加。重组TNFα的给药导致HR和HRV的双相反应，类似于LPS引起的反应。了解脓毒症期间细胞因子在异常HRV中的作用可能会导致改善在重症监护病房患者中发现威胁生命的医院感染的策略。

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