Emergency Medicine, Freeman Health System, Joplin, MO 64804, USA.
Medical Education Department, Kansas City University, Kansas City, MO 64106, USA.
Int J Mol Sci. 2024 Jul 24;25(15):8058. doi: 10.3390/ijms25158058.
The autonomic nervous system plays a key role in maintaining body hemostasis through both the sympathetic and parasympathetic nervous systems. Sympathetic overstimulation as a reflex to multiple pathologies, such as septic shock, brain injury, cardiogenic shock, and cardiac arrest, could be harmful and lead to autonomic and immunologic dysfunction. The continuous stimulation of the beta receptors on immune cells has an inhibitory effect on these cells and may lead to immunologic dysfunction through enhancing the production of anti-inflammatory cytokines, such as interleukin-10 (IL-10), and inhibiting the production of pro-inflammatory factors, such as interleukin-1B IL-1B and tissue necrotizing factor-alpha (TNF-alpha). Sympathetic overstimulation-induced autonomic dysfunction may also happen due to adrenergic receptor insensitivity or downregulation. Administering anti-adrenergic medication, such as beta-blockers, is a promising treatment to compensate against the undesired effects of adrenergic surge. Despite many misconceptions about beta-blockers, beta-blockers have shown a promising effect in decreasing mortality in patients with critical illness. In this review, we summarize the recently published articles that have discussed using beta-blockers as a promising treatment to decrease mortality in critically ill patients, such as patients with septic shock, traumatic brain injury, cardiogenic shock, acute decompensated heart failure, and electrical storm. We also discuss the potential pathophysiology of beta-blockers in various types of critical illness. More clinical trials are encouraged to evaluate the safety and effectiveness of beta-blockers in improving mortality among critically ill patients.
自主神经系统通过交感神经系统和副交感神经系统在维持身体止血方面发挥着关键作用。作为对多种病理情况（如感染性休克、脑损伤、心源性休克和心脏骤停）的反射，交感神经过度刺激可能是有害的，并导致自主和免疫功能障碍。β 受体在免疫细胞上的持续刺激对这些细胞具有抑制作用，并可能通过增强抗炎细胞因子（如白细胞介素-10 (IL-10)）的产生和抑制促炎因子（如白细胞介素-1B [IL-1B] 和组织坏死因子-α [TNF-α]）的产生导致免疫功能障碍。交感神经过度刺激引起的自主神经功能障碍也可能由于肾上腺素能受体不敏感或下调而发生。给予抗肾上腺素能药物，如β受体阻滞剂，是一种有前途的治疗方法，可以补偿肾上腺素激增的不良影响。尽管人们对β受体阻滞剂存在许多误解，但β受体阻滞剂在降低危重病患者死亡率方面显示出了有希望的效果。在这篇综述中，我们总结了最近发表的讨论使用β受体阻滞剂作为降低危重病患者死亡率的有前途的治疗方法的文章，如感染性休克、创伤性脑损伤、心源性休克、急性失代偿性心力衰竭和电风暴患者。我们还讨论了β受体阻滞剂在各种类型的危重病中的潜在病理生理学。鼓励进行更多的临床试验来评估β受体阻滞剂在改善危重病患者死亡率方面的安全性和有效性。
