Owjfard Maryam, Rahmani Negin, Mallahzadeh Arashk, Bayat Mahnaz, Borhani-Haghighi Afshin, Karimi Farzaneh, Namavar Mohammad Reza
Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Behbahan Faculty of Medical Science, Behbahan, Iran.
Heliyon. 2024 Feb 20;10(4):e26640. doi: 10.1016/j.heliyon.2024.e26640. eCollection 2024 Feb 29.
Nicorandil is a dual mechanism anti-anginal agent that acts as a nitric oxide (NO) donor and a potassium (K) channel opener. Recent studies have evaluated the effect of nicorandil on ischemic stroke. Neurons have a low tolerance to hypoxia and therefore the brain tissue is significantly vulnerable to ischemia. Current approved treatments for ischemic stroke are tissue plasminogen activators and clot retrieval methods. The narrow therapeutic time window and lack of efficacy in restoring the dying neurons urge researchers to develop an alternative approach. In the terminal stages of anoxia, K channels induce hyperpolarization in various types of neuronal cells, leading to decreased neuronal activity and the preservation of the brain's energy. Nicorandil can open these K channels and sustain the hyperpolarization phase, which may have a neuroprotective effect during hypoxia. Additionally, we review how nicorandil can improve overall stroke outcomes through its anti-inflammatory, anti-oxidative, and edema-reducing effects. One of the major components evaluated in stroke patients is blood pressure. Studies have demonstrated that the effect of nicorandil on blood pressure is related to both its K channel opening and NO donating mechanisms. Since both hypertension and hypotension need correction before stroke intervention, it's crucial to consider the role of nicorandil and its impact on blood pressure. Previously published studies indicate that the right dosage of nicorandil can improve cerebral blood flow without significant changes in hemodynamic profiles. In this review, we discuss how nicorandil may contribute to better stroke outcomes based on previously published literature and laboratory findings.
尼可地尔是一种具有双重作用机制的抗心绞痛药物，它可作为一氧化氮（NO）供体和钾（K）通道开放剂。最近的研究评估了尼可地尔对缺血性中风的影响。神经元对缺氧耐受性低，因此脑组织极易受到缺血的影响。目前批准用于缺血性中风的治疗方法是组织纤溶酶原激活剂和血栓清除方法。治疗时间窗狭窄以及在恢复濒死神经元方面缺乏疗效促使研究人员开发替代方法。在缺氧末期，钾通道可诱导各种类型神经元细胞发生超极化，导致神经元活动减少并保存大脑能量。尼可地尔可打开这些钾通道并维持超极化阶段，这在缺氧期间可能具有神经保护作用。此外，我们还综述了尼可地尔如何通过其抗炎、抗氧化和减轻水肿的作用来改善中风的总体预后。中风患者评估的主要指标之一是血压。研究表明，尼可地尔对血压的影响与其钾通道开放和一氧化氮供体机制均有关。由于在中风干预前高血压和低血压都需要纠正，因此考虑尼可地尔的作用及其对血压的影响至关重要。先前发表的研究表明，合适剂量的尼可地尔可改善脑血流量，而不会使血流动力学参数发生显著变化。在本综述中，我们根据先前发表的文献和实验室研究结果讨论尼可地尔如何有助于改善中风预后。
