Blood-oxygen-level-dependent magnetic resonance signal and cerebral oxygenation responses to brain activation are enhanced by concurrent transient hypertension in rats.
Blood-oxygen-level-dependent magnetic resonance signal and cerebral oxygenation responses to brain activation are enhanced by concurrent transient hypertension in rats.
复制标题
大鼠中并发短暂性高血压可增强血氧水平依赖性磁共振信号和对大脑激活的脑氧合反应。
DOI：
10.1038/sj.jcbfm.9600436
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Tuor,UrsulaI
中科院分区：
文献类型：
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作者：
Qiao,Min;Rushforth,Dave;Wang,Rong;Shaw,RAnthony;Tomanek,Boguslaw;Dunn,JeffF;Tuor,UrsulaI
神经元激活导致磁共振图像中血氧水平依赖性（BOLD）信号增加，脑血流量（CBF）增加和组织氧合变化。我们假设伴有神经元激活的短暂性高血压会干扰对神经元激活的正常生理反应，可能导致附加反应。麻醉的大鼠准备进行功能磁共振成像研究，测量BOLD信号的增加对：(1)前爪电刺激，(2)去甲肾上腺素引起的不同程度的短暂性高血压，以及1和2的反应。在其他类似方案的实验中，使用激光多普勒血流法和近红外光谱法测量CBF和皮质氧合血红蛋白（oxyHb）和脱氧血红蛋白（deoxyHb）的变化。前爪刺激时，感觉运动皮层内的BOLD信号增加。这与CBF和oxyHb的增加和脱氧hb的减少相匹配。在中度或重度短暂性高血压期间，BOLD信号、CBF和oxyHb存在血压依赖性增加；脱氧血红蛋白减少。当短暂性高血压和前爪刺激联合使用时，oxyHb、deoxyHb或BOLD信号的反应通常是每种反应的总和。相比之下，CBF对前爪刺激的反应相对不受短暂性高血压的影响。我们得出的结论是，在同时伴有高血压的刺激过程中，尽管CBF具有良好的自我调节，但高血压引起的组织氧合的正常变化伴随着神经元激活而增强。后者可能反映了氧气消耗的高度短暂减少，或者可能是通过更多非交换容器的流量重新分配。
Neuronal activation results in increases in blood-oxygen-level-dependent (BOLD) signal increases in magnetic resonance images, increases in cerebral blood flow (CBF), and changes in tissue oxygenation. We hypothesized that transient hypertension concurrent with neuronal activation would interfere with the normal physiological responses to neuronal activation potentially leading to additive responses. Anesthetized rats were prepared for functional magnetic resonance imaging studies in which increases in BOLD signal were measured in response to: (1) electrical forepaw stimulation, (2) different graded levels of transient hypertension produced with norepinephrine, and both 1 and 2. In other experiments with a similar protocol, changes in CBF and cortical oxyhemoglobin (oxyHb) and deoxyhemoglobin (deoxyHb) were measured using Laser Doppler Flowmetry and near-infrared (IR) spectroscopy. BOLD signal within the sensory-motor cortex increased during forepaw stimulation. These matched increases in CBF and oxyHb and decreases in deoxyHb. During moderate or severe transient hypertension, there was a blood pressure-dependent increase in BOLD signal, CBF, and oxyHb; and a decrease in deoxyHb. When transient hypertension and forepaw stimulation were combined, the responses of oxyHb, deoxyHb, or BOLD signal were generally a summation of each response. In contrast, the CBF response to forepaw stimulation was relatively unaffected by transient hypertension. We conclude that during stimulation with concurrent hypertension, the normal changes in tissue oxygenation that accompany neuronal activation are enhanced by the increases produced by hypertension despite an excellent autoregulation of CBF. The latter could reflect highly transient decreases in oxygen consumption or likely a redistribution of flow through more nonexchange vessels.