Effects of chronic psychosocial stress on cardiac autonomic responsiveness and myocardial structure in mice
Effects of chronic psychosocial stress on cardiac autonomic responsiveness and myocardial structure in mice
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DOI：
10.1152/ajpheart.00869.2003
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发表时间：
2004-06-01
影响因子：
4.8
通讯作者：
Sgoifo, A
中科院分区：
文献类型：
--
作者：
Costoli, T;Bartolomucci, A;Sgoifo, A
在每次激动性相互作用期间和之后，重复单次暴露于社会压力源会导致心脏交感迷走神经平衡向交感神经主导转变。然而，很少有证据表明慢性社会挑战可能导致持续的病理生理变化。在这项研究中，雄性 CD-1 小鼠（n = 14）被植入用于心电图记录的无线电遥测系统。我们评估了慢性心理社会压力（与优势动物进行 15 天的感觉接触和每天 5 分钟的失败发作）对 1）交感迷走神经对每次失败发作的反应的影响，通过心率变异性的时域指数（R-R 间隔、R-R 间隔的标准差和连续 R-R 间隔差异的均方根）来测量，2）整个慢性挑战中心率的昼夜节律性（夜间阶段、白天阶段和节律幅度值），以及3) 心肌结构损伤的程度（体积分数、密度和纤维化的扩展）。这项研究表明，急性心脏自主反应已形成习惯，即交感迷走平衡向交感神经主导的转变在反复失败事件中显着减少。此外，动物表现出心率节律性的显着变化，即昼夜值增加和节律幅度减小，但这些仅限于慢性社会心理压力的前 5 天。由于出现许多微观疤痕，纤维化的体积分数比对照动物大六倍。总之，尽管小鼠在急性心血管反应性和心率节律方面似乎适应了慢性社会心理压力，但结构改变发生在心肌水平。
Repeated single exposures to social stressors induce robust shifts of cardiac sympathovagal balance toward sympathetic dominance both during and after each agonistic interaction. However, little evidence is available regarding possible persistent pathophysiological changes due to chronic social challenge. In this study, male CD-1 mice (n = 14) were implanted with a radiotelemetry system for electrocardiographic recordings. We assessed the effects of chronic psychosocial stress (15-day sensory contact with a dominant animal and daily 5-min defeat episodes) on 1) sympathovagal responsiveness to each defeat episode, as measured via time-domain indexes of heart rate variability (R-R interval, standard deviation of R-R interval, and root mean square of successive R-R interval differences), 2) circadian rhythmicity of heart rate across the chronic challenge ( night phase, day phase, and rhythm amplitude values), and 3) amount of myocardial structural damage ( volume fraction, density, and extension of fibrosis). This study indicated that there was habituation of acute cardiac autonomic responsiveness, i.e., the shift of sympathovagal balance toward sympathetic dominance was significantly reduced across repeated defeat episodes. Moreover, animals exhibited significant changes in heart rate rhythmicity, i.e., increments in day and night values and reductions in the rhythm amplitude, but these were limited to the first 5 days of chronic psychosocial stress. The volume fraction of fibrosis was sixfold larger than in control animals, because of the appearance of many microscopic scarrings. In summary, although mice appeared to adapt to chronic psychosocial stress in terms of acute cardiovascular responsiveness and heart rate rhythmicity, structural alterations occurred at the myocardial level.