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人类和麻醉大鼠对呼吸暂停的功能性磁共振成像血氧水平依赖(fMRI-BOLD)信号差异反应。

Differential fMRI-BOLD signal response to apnea in humans and anesthetized rats.

作者信息

Kannurpatti Sridhar S, Biswal Bharat B, Hudetz A G

机构信息

Biophysics Research Institute, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

出版信息

Magn Reson Med. 2002 May;47(5):864-70. doi: 10.1002/mrm.10131.

DOI:10.1002/mrm.10131
PMID:11979564
Abstract

Blood oxygenation level dependent (BOLD) signal intensity (SI) and regional cerebral blood flow (CBF) during a 20-s apnea stimulus in awake humans and pentobarbital-anesthetized rats were measured to assess the usefulness of apnea in estimating cerebral vasodilatory capacity for functional MRI (fMRI) experiments. Rats were ventilated with either room air or 100% O(2.) While breathing room air, apnea for 20 s increased the BOLD SI in humans but decreased it in rats. However, in rats ventilated with 100% O(2), BOLD SI increased upon apnea for 20 s. CBF measurements in rats using laser Doppler flowmetry (LDF) showed a 45% +/- 8% increase during apnea with room air ventilation, and a 10% +/- 3% increase with 100% O(2). Arterial blood oxygen saturation fell from 96% +/- 1% to 29% +/- 5%, and cerebral tissue PO(2) decreased from 15 +/- 3 mmHg to 6 +/- 2 mmHg by the end of 20-s apnea in rats breathing room air. However, with 100% O(2) respiration, apnea produced no change in the arterial blood oxygen saturation, which remained at 99%, but increased tissue PO(2) from 35 +/- 9 mmHg to 39 +/- 10 mmHg. From the results obtained in rats ventilated with room air, it is concluded that apnea induces hypoxia that results in a decrease in fMRI-BOLD signal. The signal decrease occurred despite an increase in P(a)CO(2) and CBF. This BOLD response is the opposite of that observed in humans, who presumably do not develop hypoxia within the applied apnea period. These studies highlight the importance of the choice of ventilating gas mixture on the outcome of BOLD experiments during systemic perturbations.

摘要

在清醒人类和戊巴比妥麻醉的大鼠中,测量了20秒呼吸暂停刺激期间的血氧水平依赖(BOLD)信号强度(SI)和局部脑血流量(CBF),以评估呼吸暂停在功能性磁共振成像(fMRI)实验中估计脑血管舒张能力的有用性。用室内空气或100% O₂对大鼠进行通气。在呼吸室内空气时,20秒的呼吸暂停会增加人类的BOLD SI,但会降低大鼠的BOLD SI。然而,在用100% O₂通气的大鼠中,20秒呼吸暂停后BOLD SI会增加。使用激光多普勒血流仪(LDF)对大鼠进行的CBF测量显示,在室内空气通气的呼吸暂停期间,CBF增加了45%±8%,在100% O₂通气时增加了10%±3%。在呼吸室内空气的大鼠中,到20秒呼吸暂停结束时,动脉血氧饱和度从96%±1%降至29%±5%,脑组织PO₂从15±3 mmHg降至6±2 mmHg。然而,在100% O₂呼吸时,呼吸暂停不会使动脉血氧饱和度发生变化,仍保持在99%,但会使组织PO₂从35±9 mmHg增加到39±10 mmHg。从在呼吸室内空气的大鼠中获得的结果可以得出结论,呼吸暂停会导致缺氧,从而导致fMRI-BOLD信号降低。尽管动脉血二氧化碳分压(P(a)CO₂)和CBF增加,但信号仍会降低。这种BOLD反应与在人类中观察到的相反,人类在应用的呼吸暂停期间可能不会出现缺氧。这些研究强调了在全身扰动期间,通气气体混合物的选择对BOLD实验结果的重要性。

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