课题基金 / 基金详情

CARDIOVASCULAR AUTONOMIC CONTROL IN STRESS AND ANXIETY

CARDIOVASCULAR AUTONOMIC CONTROL IN STRESS AND ANXIETY
压力和焦虑时的心血管自主控制
批准号:
6351653
负责人:
Richard P SLOAN
金额:
$10.81万
依托单位国家:
美国
项目类别:
财政年份:
1998
资助国家:
美国
项目状态:
已结题
起止时间:
1998-04-01 至 2003-01-31

项目摘要

项目成果

Richard P SLOAN的其他基金

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中文摘要
翻译
描述(改编自申请人的摘要):这是一个应用程序 获得独立科学家奖(K 02),研究心血管自主神经 控制压力和焦虑。 它是基于一个研究计划, 重点是探讨心理/行为之间的关系 焦虑、敌意、抑郁和身体特征等 条件反射、中枢和自主神经系统以及 心血管和呼吸系统。 该申请提出了一系列实验,从一个模型, 确定血压变异性(BPV)为潜在机制, 哪些心理/精神因素和健康行为赋予 冠状动脉疾病(CAD)和灾难性心脏病的风险增加 事件 虽然有证据表明,心理因素,如焦虑, 抑郁和敌意与CAD风险增加有关, 这些因素发挥其致病作用的机制仅仅是 不太了解。 我们的模型认为心脏的自主控制 对血液振荡起缓冲或抑制作用 最近的血管生物学和动力学研究表明, 可能对内皮有致病作用, 在灾难性心脏病的情况下, 事件 我们最近已经证明,在心理条件下, 压力,这些血压振荡的幅度是相反的 与心脏的自主控制程度有关,如通过 心脏周期变异性(HPV)。 因此,在具有高水平的 心脏自主控制,血压波动最小, 在控制水平较低的受试者中,这种情况大大增加。 由于焦虑、抑郁等心理/行为特征, 和敌意与较低的HPV水平有关, 这些特征可能与血压的去抑制有关 振荡,无论是在休息,或更有可能,在响应心理 应力 总之,这些发现表明, 敌对等心理特征具有致病作用 是通过降低BPV对攻击的反应抑制, 促进动脉粥样硬化形成和斑块破裂。 在本申请中,5 提出了该模型的实验测试。
英文摘要
DESCRIPTION (Adapted from the Applicant's Abstract): This is an application for an Independent Scientist Award (K02) to study cardiovascular autonomic control in stress and anxiety. It is based on a research program whose focus is to explore the relationships among psychological/behavioral characteristics such as anxiety, hostility, depression, and physical conditioning, the central and autonomic nervous system, and the cardiovascular and respiratory systems. The application proposes a series of experiments deriving from a model which identifies blood pressure variability (BPV) as a potential mechanism by which psychological/psychiatric factors and health behaviors confer increased risk of coronary artery disease (CAD) and catastrophic cardiac events. While evidence suggests that psychological factors such as anxiety, depression, and hostility are associated with increased risk of CAD, the mechanisms by which these factors exert their pathogenic effects are only poorly understood. Our model holds that autonomic control of the heart serves a buffering or inhibitory function over oscillations in blood pressure, which recent research in vascular biology and dynamics suggests may have pathogenic effects on the endothelium, in the case of atherogenesis, and on plaque stability, in the case of catastrophic cardiac events. We recently have shown that under conditions of psychological stress, the magnitude of these blood pressure oscillations is inversely related to the degree of autonomic control of the heart, as measured by heart period variability (HPV). Thus, in subjects with high levels of cardiac autonomic control, blood pressure oscillations are minimal whereas in subjects with low levels of control, they are increased considerably. Since psychological/behavioral characteristics such as anxiety, depression, and hostility have been shown to be associated with lower levels of HPV, these characteristics may be associated with disinhibition of blood pressure oscillations, either at rest, or more likely, in response to psychological stress. Together, these findings suggest that the mechanism by which psychological characteristics such as hostility have their pathogenic effect is through reduced inhibition of BPV responses to challenge, which in turn promotes atherogenesis and plaque rupture. In this application, 5 experimental tests of this model are proposed.
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