Influence of Stroke Localization on Autonomic Activation, Immunodepression, and Post-Stroke Infection
Influence of Stroke Localization on Autonomic Activation, Immunodepression, and Post-Stroke Infection
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DOI：
10.1159/000331922
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发表时间：
2011-01-01
影响因子：
2.9
通讯作者：
Meisel, Andreas
中科院分区：
文献类型：
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作者：
Harms, Hendrik;Reimnitz, Peter;Meisel, Andreas
背景和目的：实验和临床数据表明，交感神经系统（SNS）的过度激活是中风诱导的免疫抑制的重要介质，这反过来又增加了中风后感染的易感性。在PANTHERIS（急性卒中预防性抗菌治疗）试验的事后分析中，我们研究了不同病变模式对SNS激活、免疫抑制和卒中后感染频率的影响。方法：在卒中发病后第1天测定每搏输出量、应激激素水平和免疫功能。使用阿尔伯塔卒中项目早期CT评分（ASPECTS）对卒中定位进行分级。在单变量分析中，我们研究了临床（美国国立卫生研究院卒中量表，NIHSS）和影像学卒中特征（病变体积，偏侧，定位分级）对自主神经系统活动（去甲肾上腺素，皮质醇），免疫能力（单核细胞HLA-DR表达）和卒中后感染频率的影响。在逻辑回归模型中，我们测试了可能增加中风后感染易感性的独立因素。结果如下：在单因素分析中，大的每搏输出量、影响MCA皮质不同区域的病变和SNS激活（去甲肾上腺素水平升高）与免疫功能受损（mHLA-DR表达降低）和卒中后感染的易感性增加相关。多因素分析表明去甲肾上腺素水平升高和大脑中动脉前皮质梗死是卒中后感染的独立危险因素。卒中严重程度和每搏输出量均与卒中后感染无关。结论：除了交感神经激活，我们的数据表明，大脑中动脉前皮质的缺血性病变可能是中风相关感染的主要决定因素。这一发现需要在更大规模的前瞻性研究中得到证实。版权所有（C）2011 S. Karger AG，巴塞尔
Background and Purpose: Experimental and clinical data suggest that overactivation of the sympathetic nerve system (SNS) is an essential mediator of stroke-induced immunodepression, which in turn increases susceptibility to post-stroke infections. In a post hoc analysis of the PANTHERIS (Preventive Antibacterial Treatment in Acute Stroke) trial, we investigated the impact of distinct lesion patterns on SNS activation, immunodepression, and frequency of post-stroke infections. Methods: Stroke volume, stress hormone levels, and immune function were determined on day 1 after stroke onset. Stroke localization was graded using the Alberta Stroke Programme Early CT score (ASPECTS). In univariate analysis, we investigated the impact of clinical (National Institutes of Health Stroke Scale, NIHSS) and imaging stroke characteristics (lesion volume, lateralization, localization grading) on autonomous nervous system activity (norepinephrine, cortisol), immune competence (monocytic HLA-DR expression), and the frequency of post-stroke infections. In a logistic regression model, we tested for independent factors that might increase susceptibility to post-stroke infections. Results: In a single-factor analysis, large stroke volume, lesions affecting distinct regions of the MCA cortex, and SNS activation (elevated norepinephrine levels) were associated with an impaired immune function (reduced mHLA-DR expression) and a higher susceptibility to post-stroke infections. Multivariate analysis identified increased levels of norepinephrine and infarction of the anterior MCA cortex as independent risk factors of post-stroke infections. Neither stroke severity nor stroke volume was independently associated with post-stroke infections. Conclusions: Apart from sympathetic activation, our data suggest that ischemic lesion in the anterior MCA cortex may be a major determinant of stroke-associated infection. This finding has to be confirmed in larger prospective studies. Copyright (C) 2011 S. Karger AG, Basel