摘要
背景:各种生理和病理刺激可对作过增感处理导致大量释放儿茶酚胺(CA)和交感神经系统兴奋收缩偶联和转录激发耦合随之而来的改变。 观察:已经证明,钙的氧化产物,而不是钙本身,负责这种适应新的平衡。慢性、持续性蓄积的CA及其毒性产物与心脏收缩力和重塑的抑郁有关,CA急性过度释放可能导致短暂的氧化爆发和致命性心律失常的严重损害。对这种氧化应激的反应,离子稳态失调,神经体液系统激活,免疫和炎症反应增强。这些事件是相互关联的,作为一个复杂的促进电不稳定。同样,重塑心肌细胞损失发生后引起的一proarrhythmogenic环境发展。因此,钙氧化产物可能参与触发心律失常,这是由于心肌细胞自律性和传导速度的改变引起的。与此相反,含硫氨基酸(s-aa),特别是牛磺酸及其前体半胱氨酸已被证明是调节心脏的氧化还原状态。然而,多重抗氧化性能的s-aa不大可能是专门负责他们的抗心律失常作用。他们还拥有额外的保护作用,从而稳定心脏电活动。 结论:得出具体的s-aa可以衰减超生理水平的有害影响的CA,这可以作为心律失常的治疗和/或预防的重要机制。
关键词: 含硫氨基酸,牛磺酸,半胱氨酸,儿茶酚胺,心脏毒性,心律失常,氧化损伤,心功能。
Current Medicinal Chemistry
Title:Potential of Sulphur-containing Amino Acids in the Prevention of Catecholamine-induced Arrhythmias
Volume: 25 Issue: 3
关键词: 含硫氨基酸,牛磺酸,半胱氨酸,儿茶酚胺,心脏毒性,心律失常,氧化损伤,心功能。
摘要: Background: Various physiological and pathological stimuli can hypersensitize the sympathetic nervous system resulting in a substantial release of catecholamines (CA) and consequent alterations in excitation-contraction coupling and excitation-transcription coupling.
Observations: It has been shown that oxidation products of CA, rather than CA themselves, are responsible for such adaptation to a new equilibrium. While chronic, sustained accumulation of CA and their toxic products are associated with the depression in cardiac contractile force and remodeling, acute excessive release of CA can result in brief oxidative bursts and serious damage leading in lethal arrhythmias. In response to such oxidative stress, dysregulation of ion homeostasis, activation of neurohumoral system, immune and inflammatory responses, are augmented. These events are inter-related, and as a complex promote electrical instability. Likewise, remodeling occurring after the loss of cardiomyocytes, induces the development of a proarrhythmogenic environment. Thus, CA oxidation products may be involved in triggering arrhythmias as a result of both changes in cardiac cell automaticity and conduction velocity. In contrast, sulphur-containing amino acids (S-AA), in particular taurine and its precursor cysteine have been shown to modulate redox state of the heart. However, the multiple anti-oxidant properties of S-AA are unlikely to be exclusively responsible for their anti-arrhythmic action. They also possess additional cytoprotective effects which can stabilize electrical activity of the heart.
Conclusion: It is concluded that specific S-AA may attenuate deleterious effects of supraphysiological levels of CA and this could serve as an important mechanism for the treatment and/or prevention of arrhythmogenesis.
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Cite this article as:
Potential of Sulphur-containing Amino Acids in the Prevention of Catecholamine-induced Arrhythmias, Current Medicinal Chemistry 2018; 25 (3) . https://dx.doi.org/10.2174/0929867324666170526121726
DOI https://dx.doi.org/10.2174/0929867324666170526121726 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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