Laboratory of Neuro-Organic Chemistry, Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran.
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Sci Rep. 2023 Sep 29;13(1):16401. doi: 10.1038/s41598-023-43721-7.
Extensive evidence highlights a robust connection between various forms of chronic stress and cardiovascular disease (CVD). In today's fast-paced world, with chronic stressors abound, CVD has emerged as a leading global cause of mortality. The intricate interplay of physical and psychological stressors triggers distinct neural networks within the brain, culminating in diverse health challenges. This study aims to discern the unique impacts of chronic physical and psychological stress on the cardiovascular system, unveiling their varying potencies in precipitating CVD. Twenty-one adolescent female rats were methodically assigned to three groups: (1) control (n = 7), (2) physical stress (n = 7), and (3) psychological stress (n = 7). Employing a two-compartment enclosure, stressors were administered to the experimental rats over five consecutive days, each session lasting 10 min. After a 1.5-month recovery period post-stress exposure, a trio of complementary techniques characterized by high specificity or high sensitivity were employed to meticulously evaluate CVD. Echocardiography and single-photon emission computed tomography (SPECT) were harnessed to scrutinize left ventricular architecture and myocardial viability, respectively. Subsequently, the rats were ethically sacrificed to facilitate heart removal, followed by immunohistochemistry staining targeting glial fibrillary acidic protein (GFAP). Rats subjected to psychological stress showed a wider range of significant cardiac issues compared to control rats. This included left ventricular hypertrophy [IVSd: 0.1968 ± 0.0163 vs. 0.1520 ± 0.0076, P < 0.05; LVPWd: 0.2877 ± 0.0333 vs. 0.1689 ± 0.0057, P < 0.01; LVPWs: 0.3180 ± 0.0382 vs. 0.2226 ± 0.0121, P < 0.05; LV-mass: 1.283 ± 0.0836 vs. 1.000 ± 0.0241, P < 0.01], myocardial ischemia [21.30% vs. 32.97%, P < 0.001], and neuroinflammation. This outcome underscores the imperative of prioritizing psychological well-being during adolescence, presenting a compelling avenue to curtail the prevalence of CVD in adulthood. Furthermore, extending such considerations to individuals grappling with CVD might prospectively enhance their overall quality of life.
大量证据表明,各种形式的慢性压力与心血管疾病(CVD)之间存在紧密联系。在当今快节奏的世界中,慢性压力源比比皆是,CVD 已成为全球主要的死亡原因。身体和心理压力源的复杂相互作用会在大脑中引发不同的神经网络,最终导致各种健康挑战。本研究旨在探究慢性身体和心理压力对心血管系统的独特影响,揭示它们在引发 CVD 方面的不同效力。
将 21 只青春期雌性大鼠分为三组:(1)对照组(n=7)、(2)身体应激组(n=7)和(3)心理应激组(n=7)。采用双室笼,对实验组大鼠进行连续 5 天的应激处理,每次持续 10 分钟。应激暴露后经过 1.5 个月的恢复期,采用三种具有高特异性或高敏感性的互补技术对 CVD 进行细致评估。超声心动图和单光子发射计算机断层扫描(SPECT)分别用于检查左心室结构和心肌活力。随后,安乐死大鼠以方便取出心脏,然后进行针对胶质纤维酸性蛋白(GFAP)的免疫组织化学染色。
与对照组大鼠相比,心理应激组大鼠表现出更广泛的显著心脏问题。这些问题包括左心室肥大[IVSd:0.1968±0.0163 与 0.1520±0.0076,P<0.05;LVPWd:0.2877±0.0333 与 0.1689±0.0057,P<0.01;LVPWs:0.3180±0.0382 与 0.2226±0.0121,P<0.05;LV-mass:1.283±0.0836 与 1.000±0.0241,P<0.01]、心肌缺血[21.30%与 32.97%,P<0.001]和神经炎症。这一结果强调了在青春期优先关注心理健康的重要性,为减少成年期 CVD 的患病率提供了有力途径。此外,将这些考虑因素扩展到患有 CVD 的个体,可能会前瞻性地提高他们的整体生活质量。