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慢性不可预知温和应激抑郁模型中小鼠主动脉血管反应性的改变:UCMS 导致 ACh 引起的舒张功能障碍。

Altered aortic vascular reactivity in the unpredictable chronic mild stress model of depression in mice: UCMS causes relaxation impairment to ACh.

机构信息

INSERM U930 and, Université François Rabelais de Tours, 37200 Tours, France.

出版信息

Physiol Behav. 2011 Jul 6;103(5):540-6. doi: 10.1016/j.physbeh.2011.04.002. Epub 2011 Apr 12.

Abstract

Major depression is an independent risk factor for the development of cardiovascular disease. This impact of depression on vascular function seems to be mediated by the endothelial dysfunction, defined as an impairment of endothelium-dependent vasorelaxation, which represents a reliable predictor of atherosclerosis and has been regularly found to be associated with depression. This study aimed at investigating aortic vascular reactivity in mice submitted to the unpredictable chronic mild stress (UCMS) procedure, a reliable model of depression. The results confirm the effectiveness of the UCMS procedure to induce neuroendocrine, physical and behavioral depression-like alterations as well as a significant decrease of acetylcholine-induced vasorelaxation without any effect on phenylephrine-induced vasoconstriction. In this study, we reveal an altered vascular reactivity in an animal model of depression, demonstrating an endothelial dysfunction reminiscent to the one found in depressed patients.

摘要

重度抑郁症是心血管疾病发展的一个独立风险因素。这种抑郁对血管功能的影响似乎是通过内皮功能障碍介导的,内皮功能障碍定义为内皮依赖性血管舒张功能受损,这是动脉粥样硬化的一个可靠预测因子,并且经常与抑郁症相关。本研究旨在研究接受不可预测的慢性轻度应激(UCMS)程序的小鼠的主动脉血管反应性,UCMS 程序是一种可靠的抑郁症模型。结果证实 UCMS 程序可有效诱导神经内分泌、躯体和行为抑郁样改变,以及乙酰胆碱诱导的血管舒张显著减少,而对去甲肾上腺素诱导的血管收缩无影响。在这项研究中,我们在抑郁症动物模型中发现了血管反应性的改变,表明存在类似于抑郁症患者中发现的内皮功能障碍。

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