Cardiac arrhythmias and cardiac contractility during stress: regulation by brainstem medullary raph neurons

生活是充满压力的，并且在具有易患心脏的受试者中，压力事件可能会引起突然的危及生命或致命的心律失常（心律失常）。控制心脏的神经活动是心律失常的主要触发因素。这种活动是在大脑中启动的，例如，当我们突然受到情绪冲击时。目前，负责心律失常的脑神经元的神经化学和连接尚未确定。我们的项目旨在找到这些问题的答案。我们的假设是，负责的神经元位于延髓的中线部分（大脑的下部）;这些神经元的激活将以可能引起心律失常的方式增加心脏功能;相反，它们的抑制将通过抑制潜在的致心律失常的神经信号来保护心脏。我们假设控制心脏的神经元具有血清素（大脑神经递质之一）的受体，并且神经元可以被选择性激活这些受体的特定亚型的药物抑制。我们的研究结果将通过阐明大脑中的情绪心理事件与应激诱导的心脏事件之间的联系，增加我们对心律失常原因的理解。我们的研究结果可能有助于确定在压力下保护心脏的新药。

Life is stressful, and in subjects with predisposed hearts stressful events may provoke sudden life-threatening or fatal disturbances of the heart rhythm (arrhythmias). Activity in nerves that control the heart is the main trigger of arrhythmias. This activity is initiated in the brain, when, for example, we have a sudden emotional shock. At present, the neurochemistry and connections of the brain neurons responsible for arrhythmias, have not been identified. Our project is designed to find answers to these questions. Our hypothesis is that the responsible neurons are located in the midline portion of the medulla oblongata (the lower part of the brain); that activation of these neurons will increase cardiac function in a manner that may provoke arrhythmias; and, conversely, that their inhibition will protect the heart during stressful events by suppressing potentially arrhythmogenic neural signals. We hypothesise that cardiac-controlling neurons possess receptors for serotonin (one of the brain neurotransmitters), and that the neurons can be inhibited by drugs that selectively activate a specific subtype of these receptors. Our results will increase our understanding of the causes of cardiac arrhythmias by elucidating the link between emotional-psychological events in the brain and stress-induced cardiac events. Our findings could contribute to the identification of new drugs that will protect the heart during stress.