组成图示
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传感器类型
其他（基于T2* MRI的氧代谢生物传感器）
检测对象
组织氧利用/代谢（tissue oxygen utilization/metabolism）、氧合血红蛋白/脱氧血红蛋白比例（oxyhemoglobin:deoxyhemoglobin ratio）；样品基质：大鼠脑组织（永久MCAO缺血脑）
检测原理
吸入100% O2的氧挑战使血浆游离O2升高。在仍有血流和代谢的脑组织中，O2被组织摄取，血红蛋白释放O2后形成顺磁性脱氧血红蛋白（deoxy-Hb）；OC期间游离O2可维持或恢复抗磁性氧合血红蛋白（oxy-Hb），降低局部deoxy-Hb浓度，减少红细胞周围磁场不均匀，使T2*加权信号升高。组织氧利用或氧提取分数越高，基线deoxy-Hb越多，OC后T2*升高越明显；缺血核心因血流和代谢丧失，T2*变化很小。信号由EPI或FLASH T2*序列采集，经SPM/GLM统计并与DWI/ASL配准，从而将代谢活跃区与不活跃区区分。
检测灵敏度
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效应效果
两组各5只大鼠显示OC可区分代谢状态：第一组PWI/DWI不匹配区T2*升高3.7%±1.4%，显著高于对侧皮层1.8%±0.68%，缺血核心仅0.24%±0.42%；ADC病灶内阳性区约3.5%±2.4%。第二组FLASH与组织学配准显示边缘区4.9%±2.5%，缺血核心0.7%±2%，正常同侧皮层3.5%±1.4%。ASL显示OC未显著改变边缘区CBF（-0.008，95% CI -0.066至0.081，P=0.78），提示T2*变化主要反映代谢而非血流。与PWI/DWI mismatch相比，OC提供氧利用信息，作者认为可更精确界定半暗带并具临床潜力。
传感器的构成
- 换能器/检测系统：Bruker Biospec 7T/30 cm MRI系统，72 mm鸟笼谐振器与2 cm线性表面接收线圈，用于产生磁场并接收T2*信号
- 刺激/调制源：氧挑战（OC），30% O2基线、100% O2 5 min 20 s，提高血浆游离O2并改变血红蛋白氧合状态
- 识别/传感介质：内源性血红蛋白（Hb），氧合血红蛋白（oxy-Hb，抗磁性）与脱氧血红蛋白（deoxy-Hb，顺磁性）作为氧利用指示物
- 样品/组织基质：大鼠脑组织，永久MCAO模型，包含缺血核心、边缘区/半暗带和对侧正常皮层
- 成像序列：单-shot梯度回波EPI T2*（TE 20 ms，TR 10 s）或FLASH 2D T2*（TE 21.4 ms，TR 317.7 ms），采集OC期间T2*变化
- 辅助定位层：DWI/ADC、ASL/PWI、RARE T2及H&E组织学，用于定义ROI、配准和验证代谢区
- 统计读出：SPM统计参数映射、GLM和AIR配准，输出T2*信号变化百分比及显著性图
中文摘要
本文报道一种新型磁共振成像技术，通过氧挑战（OC，5 min 100% O2）期间氧合血红蛋白与脱氧血红蛋白比例及T2*信号变化间接检测组织代谢。OC期间T2*信号升高反映O2与脱氧血红蛋白结合，而脱氧血红蛋白由摄取氧的代谢组织产生。作者将OC用于识别缺血脑内组织代谢。在大鼠中诱导永久性大脑中动脉闭塞（MCAO）。第一组（n=5）先进行扩散加权成像（DWI），再在OC期间采集平面回波T2*，并进行灌注加权成像（PWI，动脉自旋标记）。OC使对侧皮层、PWI/DWI不匹配区同侧皮层和缺血核心的T2*信号分别升高1.8%、3.7%和0.24%。T2*与表观扩散系数（ADC）图配准显示T2*升高延伸至ADC病灶内（3.4%）。第二组（n=5）将FLASH T2*和ADC图与组织学配准，显示组织学定义边缘区（55%正常神经元形态，位于ADC病灶边界内）T2*升高4.9%，而皮层缺血核心（92%神经元缺血性细胞改变，核心ADC病灶）仅升高0.7%。OC具有潜在临床价值，可通过区分低灌注区内代谢活跃与不活跃组织，更精确评估半暗带。
英文摘要
We describe a novel magnetic resonance imaging technique for detecting metabolism indirectly through changes in oxyhemoglobin:deoxyhemoglobin ratios and T2(*) signal change during 'oxygen challenge' (OC, 5 mins 100% O(2)). During OC, T2(*) increase reflects O(2) binding to deoxyhemoglobin, which is formed when metabolizing tissues take up oxygen. Here OC has been applied to identify tissue metabolism within the ischemic brain. Permanent middle cerebral artery occlusion was induced in rats. In series 1 scanning (n=5), diffusion-weighted imaging (DWI) was performed, followed by echo-planar T2(*) acquired during OC and perfusion-weighted imaging (PWI, arterial spin labeling). Oxygen challenge induced a T2(*) signal increase of 1.8%, 3.7%, and 0.24% in the contralateral cortex, ipsilateral cortex within the PWI/DWI mismatch zone, and ischemic core, respectively. T2(*) and apparent diffusion coefficient (ADC) map coregistration revealed that the T2(*) signal increase extended into the ADC lesion (3.4%). In series 2 (n=5), FLASH T2(*) and ADC maps coregistered with histology revealed a T2(*) signal increase of 4.9% in the histologically defined border zone (55% normal neuronal morphology, located within the ADC lesion boundary) compared with a 0.7% increase in the cortical ischemic core (92% neuronal ischemic cell change, core ADC lesion). Oxygen challenge has potential clinical utility and, by distinguishing metabolically active and inactive tissues within hypoperfused regions, could provide a more precise assessment of penumbra.