Nakada K, Yoshida D, Fukumoto M, Yoshida S
Department of Radiology, Kochi Medical School, Okoh, Nankoku, Kochi 783-8505, Japan.
J Magn Reson Imaging. 2001 Mar;13(3):344-51. doi: 10.1002/jmri.1049.
The purpose of this study was to examine which physiological factors affect cerebral T2* signal intensity (SI) during breath holding (BH) (apnea after inspiration and breathing after expiration) in normal volunteers. We examined SI changes caused by anoxic gas inhalation, by respiratory movements, and by BH. High-speed echo planar images (EPI) showed changes in SI that could be divided into five phases. Reports indicate that SI changes induced by BH are due to the effects on the magnetic susceptibility of deoxygenated hemoglobin (deoxyhemoglobin (dHb)) and to hypercapnia, but these reports could not fully explain the observed five phases. In addition to deoxyhemoglobin susceptibility and hypercapnia, we found that respiratory movements play a third critical role in modifying SI by affecting blood flow into the region of interest (ROI), as judged from right carotid artery flow. Consequently, we propose that the physiological SI changes induced by BH are derived from blood oxygenation, hypercapnia, and respiratory movements.
本研究的目的是在正常志愿者中，检测在屏气（BH）（吸气后屏气和呼气后呼吸）过程中，哪些生理因素会影响脑T2*信号强度（SI）。我们检测了由吸入缺氧气体、呼吸运动和屏气引起的SI变化。高速回波平面成像（EPI）显示SI的变化可分为五个阶段。报告表明，屏气引起的SI变化是由于对脱氧血红蛋白（dHb）的磁化率的影响以及高碳酸血症，但这些报告无法完全解释观察到的五个阶段。除了脱氧血红蛋白磁化率和高碳酸血症外，我们发现呼吸运动通过影响进入感兴趣区域（ROI）的血流，在改变SI方面起着第三个关键作用，这是根据右颈动脉血流判断得出的。因此，我们提出屏气引起的生理性SI变化源自血液氧合、高碳酸血症和呼吸运动。
