Introduction. In the animal model, preconditioning is a powerful weapon against ischemic damage. The reason why the human heart cannot be protected from ischemic damage by preconditioning remains unclear. There are assumptions that the lack of preconditioning in humans is caused by concomitant diseases such as dyslipoproteinemia and arteriosclerosis. This study investigates whether dyslipoproteinemia and the resulting arteriosclerosis can be a cause of a reduced precondition effect of heart in mice. Methods. LDL receptor-deficient mice were fed a long-term (14-16 weeks) high-fat atherogenic diet to induce arteriosclerosis. Arteriosclerosis was identified by histological examination and vessel contraction tests. LDLR-/- and wild-type mice were randomly assigned to anesthetic-induced, remote ischemic, or no preconditioning. All mice were subjected to 45 minutes of coronary artery occlusion and 180 minutes of reperfusion. The area at risk and infarct size were determined by Evans Blue and triphenyltetrazolium chloride staining. Results. Histopathological examination showed atherosclerosis in high-fat atherogenic fed LDLR-/- mice, and the vessel relaxation capacity was significantly reduced compared to wild-type mice. In the wild type, as expected, infarct size was significantly reduced by preconditioning compared to the control. In LDLR-/- mice, infarct size was significantly reduced by preconditioning compared to the control. Surprisingly, the LDLR-/- control group also had a significantly reduced infarct size compared to the wild-type control group. Conclusion. We were able to demonstrate that a high-fat diet morphologically and functionally triggered atherosclerosis in LDLR-/- mice. Interestingly, LDLR-/- mice with an atherogenic diet had smaller infarct sizes compared to wild-type mice. Moreover, preconditioning additionally reduced myocardial infarct size in LDLR-/- mice. A long-term high-fat atherogenic diet and preconditioning seem to result in additive cardioprotection in LDLR-/- mice.

中文翻译：

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体内动脉粥样硬化低密度脂蛋白受体-/- 小鼠体内保留了远程和麻醉诱导的心肌预处理

简介。在动物模型中，预处理是对抗缺血性损伤的有力武器。预处理不能保护人类心脏免受缺血性损伤的原因仍不清楚。有假设认为，人类缺乏预处理是由伴随疾病引起的，例如异常脂蛋白血症和动脉硬化。本研究调查异常脂蛋白血症和由此产生的动脉硬化是否可能是小鼠心脏先决条件效应降低的原因。方法. 长期（14-16 周）喂食 LDL 受体缺陷小鼠高脂肪致动脉粥样硬化饮食以诱发动脉硬化。通过组织学检查和血管收缩试验确定动脉硬化。LDLR-/- 和野生型小鼠被随机分配到麻醉诱导、远程缺血或无预处理组。对所有小鼠进行 45 分钟的冠状动脉闭塞和 180 分钟的再灌注。通过伊文思蓝和氯化三苯四唑染色确定危险区域和梗塞面积。结果. 组织病理学检查显示，喂食高脂致动脉粥样硬化的LDLR-/-小鼠出现动脉粥样硬化，与野生型小鼠相比，血管舒张能力显着降低。在野生型中，正如预期的那样，与对照相比，预处理显着减少了梗塞面积。在 LDLR-/- 小鼠中，与对照组相比，预处理显着减少了梗塞面积。令人惊讶的是，与野生型对照组相比，LDLR-/- 对照组的梗死面积也显着减小。结论. 我们能够证明高脂肪饮食在形态和功能上引发了 LDLR-/- 小鼠的动脉粥样硬化。有趣的是，与野生型小鼠相比，采用致动脉粥样硬化饮食的 LDLR-/- 小鼠的梗塞面积更小。此外，预处理还减少了 LDLR-/- 小鼠的心肌梗死面积。长期的高脂肪致动脉粥样硬化饮食和预处理似乎可以对 LDLR-/- 小鼠产生额外的心脏保护作用。