关键词: GPCR adenosine receptors fainting neuropeptide Y syncope vagus nerve

Mesh : Humans Syncope / physiopathology Animals Heart / physiopathology Brain / physiopathology metabolism Neurons / metabolism Signal Transduction

来  源:   DOI:10.3390/ijms25136959   PDF(Pubmed)

Abstract:
Observed and recorded in various forms since ancient times, \'syncope\' is often popularly called \'fainting\', such that the two terms are used synonymously. Syncope/fainting can be caused by a variety of conditions, including but not limited to head injuries, vertigo, and oxygen deficiency. Here, we draw on a large body of literature on syncope, including the role of a recently discovered set of specialized mammalian neurons. Although the etiology of syncope still remains a mystery, we have attempted to provide a comprehensive account of what is known and what still needs to be performed. Much of our understanding of syncope is owing to studies in the laboratory mouse, whereas evidence from human patients remains scarce. Interestingly, the cardioinhibitory Bezold-Jarisch reflex, recognized in the early 1900s, has an intriguing similarity to-and forms the basis of-syncope. In this review, we have integrated this minimal model into the modern view of the brain-neuron-heart signaling loop of syncope, to which several signaling events contribute. Molecular signaling is our major focus here, presented in terms of a normal heart, and thus, syncope due to abnormal or weak heart activity is not discussed in detail. In addition, we have offered possible directions for clinical intervention based on this model. Overall, this article is expected to generate interest in chronic vertigo and syncope/fainting, an enigmatic condition that affects most humans at some point in life; it is also hoped that this may lead to a mechanism-based clinical intervention in the future.
摘要:
自古以来以各种形式观察和记录,“晕厥”通常被称为“昏厥”,这两个术语是同义使用的。晕厥/昏厥可由多种情况引起,包括但不限于头部受伤,眩晕,和缺氧。这里,我们借鉴了大量关于晕厥的文献,包括最近发现的一组专门的哺乳动物神经元的作用。虽然晕厥的病因仍然是个谜,我们试图全面说明已知的内容和仍需要执行的内容。我们对晕厥的大部分理解是由于对实验室老鼠的研究,而来自人类患者的证据仍然很少。有趣的是,心脏抑制Bezold-Jarisch反射,在1900年代初认识到,与晕厥有着有趣的相似性,并形成了晕厥的基础。在这次审查中,我们已经将这个最小模型整合到晕厥的大脑-神经元-心脏信号回路的现代视图中,几个信令事件对此有贡献。分子信号是我们的主要关注点,以正常的心脏表示,因此,不详细讨论由于心脏活动异常或虚弱引起的晕厥。此外,我们基于该模型为临床干预提供了可能的指导.总的来说,这篇文章有望引起人们对慢性眩晕和晕厥/晕厥的兴趣,一种神秘的疾病,在生命的某个时候影响大多数人;人们也希望这可能导致未来基于机制的临床干预。
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