Social interaction modulates autonomic, inflammatory, and depressive-like responses to cardiac arrest and cardiopulmonary resuscitation
Social interaction modulates autonomic, inflammatory, and depressive-like responses to cardiac arrest and cardiopulmonary resuscitation
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DOI：
10.1073/pnas.1007583107
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发表时间：
2010-09-14
影响因子：
11.1
通讯作者：
DeVries, A. Courtney
中科院分区：
文献类型：
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作者：
Norman, Greg J.;Zhang, Ning;DeVries, A. Courtney
心理因素，包括抑郁和社会孤立，是心血管健康的重要决定因素。本研究使用一种经过验证的心跳骤停/心肺复苏(CA/CPR)小鼠模型来研究社会环境对脑缺血的几种病理生理和行为反应的影响。在实验期间，雄性实验小鼠要么与去卵巢的雌性小鼠成对饲养，要么在社会上被隔离。心脏骤停增加了促炎细胞因子TNF-α、IL-1β和IL-6以及小胶质细胞标志物MAC-1的mRNA表达；除IL-6外，这些因子在社交隔离小鼠中的表达进一步增加。此外，暴露在CA/CPR程序中的社交隔离动物在手术后7天显示出显著更高水平的神经细胞死亡和海马区小胶质细胞染色。社会隔离也加剧了CA/CPR诱导的抑郁样行为和心脏自主神经失调。在没有缺血性损伤的情况下，社会环境对神经细胞死亡、自主心脏控制或行为的表达没有显著影响。综上所述，这些数据表明，社会因素影响心脏骤停后的病理生理轨迹。
Psychological factors, including depression and social isolation, are important determinants of cardiovascular health. The current study uses a well-validated mouse model of cardiac arrest/cardiopulmonary resuscitation (CA/CPR) to examine the effect of social environment on several pathophysiological and behavioral responses to cerebral ischemia. Male experimental mice were either housed in pairs with an ovariectomized female or socially isolated for the duration of the experiment. Cardiac arrest increased the mRNA expression of the proinflammatory cytokines TNF-alpha, IL-1 beta, and IL-6, as well as the microglia marker MAC-1; expression of each of these factors, except IL-6, was further increased among socially isolated mice. Furthermore, socially isolated animals exposed to the CA/CPR procedure displayed significantly higher levels of neuronal cell death and microglia staining within the hippocampus at 7 d following surgery. Social isolation also exacerbated CA/CPR-induced depressive-like behavior and cardiac autonomic dysregulation. In the absence of ischemic damage, social environment had no significant effect on the expression of neuronal cell death, autonomic cardiac control, or behavior. Together, these data suggest that social factors influence the pathophysiological trajectory following cardiac arrest.