慢性社会心理压力是公认的但尚未得到充分研究的心脏病危险因素，具有潜在的性别特异性影响。我们研究了慢性应激是否会在遭受缺血再灌注损伤的离体 Wistar 大鼠心脏中引发性别依赖性心功能障碍。与匹配的对照组相比，实验队列每天接受 1 小时的束缚压力，持续 4 周，然后进行安乐死（戊巴比妥钠）和心脏切除进行离体灌注。血液分析揭示了应激激素和炎症标志物的性别特异性变化。与对照组相比，慢性束缚应激（CRS）男性的血浆脑源性神经营养因子（BDNF）水平降低（p<0.05），而CRS女性则表现出血浆促肾上腺皮质激素（ACTH）升高（p<0.01）和皮质酮降低（p<0.01）。 <0.001），同时降低血清雌二醇（p<0.001）和雌二醇/孕酮比率（p<0.01）。值得注意的是，CRS 女性表现出血清心肌肌钙蛋白 T (p<0.05) 和肿瘤坏死因子-α (TNF-a) (p<0.01) 升高，同时白细胞介素 (IL)-1a、IL-1β、IL-6 和 IL-6 受到抑制。与对照组相比，IL-10 水平 (p<0.05)。离体 Langendorff 灌注显示，CRS 女性心脏在基线每搏输出量 (p<0.01)、工作表现 (p<0.05)、主动脉输出量 (p<0.05)、冠状动脉流量 (p<0.01) 等方面表现出缺血后功能恢复受损。与匹配对照和 CRS 男性相比 (p<0.05) 和总心输出量 (p<0.01)。我们的研究结果揭示了应激心脏在系统和功能水平上的有趣的性别特异性反应。在这里，应激激素的失调、促炎症状态和女性在应激方案后潜在的潜在心肌病使她们在心肌缺血后更容易受到损伤。这项研究强调了将性别作为生物学变量纳入关注应激相关心肌病的心脏研究的重要性。

Chronic psychosocial stress is a recognized, yet understudied risk factor for heart disease, with potential sex-specific effects. We investigated whether chronic stress triggers sex-dependent cardiac dysfunction in isolated Wistar rat hearts subjected to ischemia-reperfusion injury. The experimental cohort underwent 1 hour of daily restraint stress for four weeks versus matched controls, followed by euthanasia (sodium pentobarbitone) and heart excision for ex vivo perfusion. Blood analysis revealed sex-specific alterations in stress hormones and inflammatory markers. Compared to controls, chronic restraint stress (CRS) males displayed decreased plasma brain-derived neurotrophic factor (BDNF) levels (p<0.05), while CRS females exhibited elevated plasma adrenocorticotropic hormone (ACTH) (p<0.01) and reduced corticosterone (p<0.001) alongside lower serum estradiol (p<0.001) and estradiol/ progesterone ratio (p<0.01). Of note, CRS females showed increased serum cardiac troponin T (p<0.05) and tumor necrosis factor-alpha (TNF-a) (p<0.01) with suppressed interleukin (IL)-1a, IL-1β, IL-6, and IL-10 levels (p<0.05) when compared to controls. Ex vivo Langendorff perfusions revealed that CRS female hearts displayed impaired post-ischemic functional recovery for baseline stroke volume (p<0.01), work performance (p<0.05), aortic output (p<0.05), coronary flow (p<0.01), and overall cardiac output (p<0.01) when compared to matched controls and CRS males (p<0.05). Our findings reveal intriguing sex-specific responses at both the systemic and functional levels in stressed hearts. Here, the dysregulation of stress hormones, pro-inflammatory state, and potential underlying cardiomyopathy in females following the stress protocol renders them more prone to damage following myocardial ischemia. This study emphasizes the importance of incorporating sex as a biological variable in cardiac research focusing on stress-related cardiomyopathy.