AUTONOMIC CARDIOVASCULAR CONTROL IN ANXIETY AND STRESS

在这份修订后的ADAMHA科学家发展奖申请表中 (I级)，提出了一个有监督的培训和研究方案，以 自主神经系统(ANS)对心血管功能调控的研究 焦虑和心理压力。总体目标是学习 大脑如何在心理状态下控制心血管系统 压力。杰克·戈尔曼博士将担任该计划的负责人。这个 应聘者将接受HR、BP和呼吸信号方面的指导 理查德·科恩和J·科恩博士的处理、分析和建模。 Thomas Bigger，并将这些方法应用于几个进行的实验 在他们的监督下。此外，应聘者还将参加课程 神经科学、神经解剖学和工程行为以及另外两个 在Harold Sackeim博士的监督下进行的研究，以评估 大脑皮层下行对心率、血压和血压调节机制的影响 呼吸。 ANS控制是正常心血管对心理反应的基础 压力，以及控制的失调被广泛假设为起作用 在各种精神和心血管疾病的病理生理学中的作用 精神错乱。例如，夸大的血流动力学反应 具有挑战性的事件被认为是处于危险中的正常个人的特征 适用于冠心病(CHD)[1]以及恐慌患者 障碍(PD)[2，3]。尽管有证据表明ANS紊乱 在这些情况下心血管功能的调节，其起源 其中一些夸张的反应并没有得到很好的理解。 最近，几种非侵入性方法评估ANS 心血管控制已经被开发用于人类 学习。一种这样的方法使用节拍到节拍变异性的分析 生物信号，主要是心率(HR)[4=-7]，以模拟 心血管控制系统。这种方法得到了广泛的应用。 医学[8，01]，新生儿科[10，11]，老年学[12，13]，以及 心脏病学[14，18]和最近介绍的精神病学[19，20]。 其他提供信息的方法已经利用了临床上派生的“自然” ECT实验、单侧脑失活、中风和 研究心脏移植对心脏收缩功能下降的影响。 因此，在此应用程序中，候选人建议使用新的 研究变异函数ANS控制的信号处理方法 正常受试者在实验室中的心理应激状态 在各种条件下和在工作现场。 对接受WADA程序和ECT的患者的更多研究将 评价变异系数下降控制条件下的变异系数调节 监管被打乱了。这些研究将得到以下补充 神经科学方面的课程。总而言之，这些方法将是有用的 在阐明对焦虑的血流动力学反应的潜在机制 和心理压力。 因此，本提案的总体目标是研究自主神经。 控制心率、血压和呼吸反应 对焦虑背后的血流动力学影响的理解 回应。了解这些效应的机制可能会导致 治疗和预防方面的进展。

In this revised application for an ADAMHA Scientist Development Award (Level I), a program of supervised training and research is proposed to study autonomic nervous system (ANS) control of cardiovascular function in anxiety and psychological stress. The overall objective is to learn how the brain controls the cardiovascular system during psychological stress. Dr. Jack Gorman will be the preceptor of the program. The candidate will receive instruction in HR, BP, and respiration signal processing, analysis, and model building from Drs. Richard Cohen and J. Thomas Bigger and apply these approaches in several experiments conducted under their supervision. In addition, the candidate will take courses in neuroscience, neuroanatomy, and engineering conduct and two other studies, under the supervision of Dr. Harold Sackeim, to evaluate descending cortical influences on ANS control mechanisms of HR, BP, and respiration. ANS control underlies the normal cardiovascular response to psychological stress, and dysregulation of the control is widely hypothesized to play a role in the pathophysiology of various psychiatric and cardiovascular disorders. For example, exaggerated hemodynamic responsiveness to challenging events is thought to characterize normal individuals at risk for coronary heart disease (CHD) [1] as well as patients with panic disorder (PD) [2,3]. Despite evidence suggesting disordered ANS regulation of cardiovascular function in these conditions, the origins of the exaggerated responses are not well understood. Recently, several noninvasive approaches to assessment of ANS cardiovascular control have been developed for application to human studies. One such approach employs analysis of beat-to-beat variability of biological signals, primarily heart rate (HR) [4=-7], to model the cardiovascular control system. This approach has had wide application in medicine [8, 01], neonatology [10, 11], gerontology [12, 13], and cardiology [14, 18] and more recent introduction in psychiatry [19, 20]. Other informative approaches have utilized clinically derived "natural experiments" of ECT, unilateral cerebral inactivation, stroke, and cardiac transplantation to study descending influences on CV regulation. Accordingly, in this application, the candidate proposes to use new signal processing approaches to investigate ANS control of CV function under psychological stress in normal subjects in the laboratory under various conditions and at the worksite. Additional studies of patients undergoing the Wada procedure and ECT will asses CV regulation under conditions in which descending control of CV regulation is disrupted. These studies will be supplemented with coursework in neuroscience. Together, these approaches will be useful in elucidating the mechanisms underlying hemodynamic responses to anxiety and psychological stress. Thus, the overall objective of this proposal is to study autonomic control of heart rate, blood pressure, and respiratory responses toward an understanding of the hemodynamic effects underlying the anxious response. Understanding the mechanisms of these effects may lead to advances in treatment and prophylaxis.