Methylene blue potentiates stimulus-evoked fMRI responses and cerebral oxygen consumption during normoxia and hypoxia.
Methylene blue potentiates stimulus-evoked fMRI responses and cerebral oxygen consumption during normoxia and hypoxia.
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DOI：
10.1016/j.neuroimage.2013.01.027
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发表时间：
2013-05-15
期刊：
影响因子：
5.7
通讯作者：
Duong TQ
中科院分区：
文献类型：
--
作者：
Huang S;Du F;Shih YY;Shen Q;Gonzalez-Lima F;Duong TQ
亚甲基蓝USP（MB）在低剂量下具有代谢增强和抗氧化特性，并表现出实验性神经治疗益处，但其对脑血流量（CBF）、功能性诱发反应和脑氧消耗代谢率（CMRO 2）相关变化的体内影响知之甚少。本研究使用磁共振成像（MRI）评价了单次静脉注射MB治疗剂量（0.5 mg/kg）对基础CBF、血氧水平依赖性（BOLD）和高碳酸血症（空气中5% CO2）吸入引起的CBF反应的体内影响，以及大鼠大脑前爪刺激期间BOLD、CBF和CMRO 2的变化。我们发现，该MB治疗剂量对动脉血氧饱和度、心率和fMRI对高碳酸血症的反应没有显著影响。然而，MB显着增强前蹄诱发的BOLD和CBF的变化在常氧下。为了进一步评价MB在代谢应激条件下的体内作用，还在轻度缺氧（15%O2）下进行了MRI测量。缺氧本身增加诱发的功能性MRI反应。MB在缺氧条件下进一步增强前蹄诱发的BOLD，CBF和氧消耗反应相对于常氧。这些发现为MB对体内脑血流动力学的影响提供了见解，并有助于优化线粒体功能障碍和氧化应激神经系统疾病的治疗。
Methylene blue USP (MB) at low doses has metabolic-enhancing and antioxidant properties and exhibits experimental neurotherapeutic benefits, but little is known about its in vivo effects on cerebral blood flow (CBF), functional evoked responses, and the associated changes in cerebral metabolic rate of oxygen consumption (CMRO2). This study used magnetic resonance imaging (MRI) to evaluate the in vivo effects of a single intravenous MB therapeutic dose (0.5 mg/kg) on basal CBF, blood oxygenation level-dependent (BOLD) and CBF responses to hypercapnic (5% CO2 in air) inhalation, as well as changes in BOLD, CBF, and CMRO2 during forepaw stimulation in the rat brain. We found that this MB therapeutic dose did not have significant effects on arterial oxygen saturation, heart rate and fMRI responses to hypercapnia. However, MB significantly potentiated forepaw-evoked BOLD and CBF changes under normoxia. To further evaluate in vivo effects of MB under metabolic stress conditions, MRI measurements were also made under mild hypoxia (15% O2). Hypoxia per se increased evoked functional MRI responses. MB under hypoxia further potentiated forepaw-evoked BOLD, CBF and oxygen consumption responses relative to normoxia. These findings provide insights into MB’s effects on cerebral hemodynamics in vivo and could help to optimize treatments in neurological diseases with mitochondrial dysfunction and oxidative stress.
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