Plante Gérard E
Department of Medicine (Nephrology), Institute of Geriatrics, University of Sherbrooke, Quebec, Canada.
Metabolism. 2005 May;54(5 Suppl 1):45-8. doi: 10.1016/j.metabol.2005.01.013.
Until relatively recently, depression has been considered a purely "mental" disorder and therefore in the natural domain of psychologists and psychiatrists. However, recent epidemiological studies have revealed that aging, physical and psychological stress, chronic pain, several metabolic disorders such as insulin resistance and established diabetes, alcoholism, inflammatory conditions, and vascular disorders such as arterial hypertension all may be associated with depression. The present review examines some of these depression-associated factors and the mechanisms by which they might give rise to vascular disorders such as atherosclerosis, microcirculation endothelial dysfunction, and interstitial disturbances leading to organ damage. A number of disorders involving the circulation can lead progressively and insidiously to large artery rigidity, remodeling of peripheral arteries, and alterations of the microcirculation of large blood vessels. Perturbations in vasa vasorum blood flow may contribute to atherogenesis, in addition to the influence of numerous cellular events involved in inflammation (tumor necrosis factor alpha, interleukin 1 beta, etc). Since Hans Selye first described the neuroendocrine cascade generated by experimentally induced stress half a century ago, phenomena such as the axonal release of neurotransmitters (including serotonin), accumulation of metabolites such as homocysteine, platelet-activating factor, and nitric oxide also have been implicated in the pathogenesis of depression. Moreover, vascular consequences of depression such as heart rate and pulse pressure variations may lead to endothelial dysfunction in critical microcirculation networks (cerebral, myocardial, and renal) and initiate physicochemical alterations in interstitial compartments adjacent to vital organs. The appropriate use of ambulatory monitoring of vascular parameters, such as heart rate and pulse pressure, and eventually, early identification of genetic and metabolic markers may prove helpful in the early detection of events preceding and predicting the clinical manifestations of depression.
直到最近，抑郁症一直被视为一种纯粹的“精神”障碍，因此属于心理学家和精神科医生的自然研究领域。然而，最近的流行病学研究表明，衰老、身体和心理压力、慢性疼痛、几种代谢紊乱（如胰岛素抵抗和已确诊的糖尿病）、酗酒、炎症性疾病以及血管疾病（如动脉高血压）都可能与抑郁症有关。本综述探讨了其中一些与抑郁症相关的因素，以及它们可能导致血管疾病（如动脉粥样硬化、微循环内皮功能障碍和导致器官损伤的间质紊乱）的机制。许多涉及循环系统的疾病会逐渐且隐匿地导致大动脉僵硬、外周动脉重塑以及大血管微循环改变。除了炎症中涉及的众多细胞事件（肿瘤坏死因子α、白细胞介素1β等）的影响外，血管滋养血管血流的扰动可能有助于动脉粥样硬化的发生。自从汉斯·塞利半个世纪前首次描述实验性诱导应激产生的神经内分泌级联反应以来，诸如神经递质（包括血清素）的轴突释放、同型半胱氨酸、血小板活化因子和一氧化氮等代谢产物的积累等现象也被认为与抑郁症的发病机制有关。此外，抑郁症的血管后果（如心率和脉压变化）可能导致关键微循环网络（脑、心肌和肾）的内皮功能障碍，并引发重要器官相邻间质隔室的物理化学改变。适当使用动态监测血管参数（如心率和脉压），最终早期识别遗传和代谢标志物，可能有助于早期发现抑郁症临床表现之前的事件并进行预测。
