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麻醉大鼠的基线生理状态及对呼吸暂停的功能磁共振成像血氧水平依赖信号反应

Baseline physiological state and the fMRI-BOLD signal response to apnea in anesthetized rats.

作者信息

Kannurpatti Sridhar S, Biswal Bharat B, Hudetz A G

机构信息

Department of Radiology, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA.

出版信息

NMR Biomed. 2003 Aug;16(5):261-8. doi: 10.1002/nbm.842.

Abstract

To decipher the biophysical mechanism behind the fMRI-BOLD response to apnea and its dependence on the baseline cerebral blood flow and oxygenation, fMRI and laser Doppler flow (LDF) studies were carried out in anesthetized rats. Baseline cerebral blood flow (CBF) and PaO2 were modulated by ventilating with different gas mixtures namely, room air (21% O2), 100% O2, carbogen (95% O2+5% CO2), 2% CO2 in air or 5% CO2 in air, respectively. A decrease in BOLD signal intensity was observed after the onset of apnea with either room air, 2% CO2 or 5% CO2 ventilation. PaO2 and cerebral tissue PO2 decreased during apnea under these conditions. However, the apnea-induced BOLD signal intensity was unaffected with carbogen ventilation and increased with 100% O2 ventilation, during which PaO2 remained constant and cerebral tissue PO2 increased. When baseline CBF was high during hypercapnia, a faster decrease occurred in the apnea-induced BOLD signal. Apnea induced the largest increase in CBF of 85 +/- 25% when ventilated with 2% CO2 while a 44 +/- 8% increase was observed with room air. During the other ventilatory conditions, minimal or no significant change in CBF was observed during apnea. These results show a significant correlation between the BOLD signal change and tissue PO2 in response to apnea under different physiological conditions. Apnea-induced increase in CBF affects the magnitude of the BOLD signal response when PaO2 remains constant or changes minimally.

摘要

为了解功能性磁共振成像血氧水平依赖(fMRI-BOLD)对呼吸暂停反应背后的生物物理机制及其对基线脑血流量和氧合的依赖性,在麻醉大鼠中进行了fMRI和激光多普勒血流(LDF)研究。通过分别用不同的气体混合物进行通气来调节基线脑血流量(CBF)和动脉血氧分压(PaO2),这些气体混合物分别为室内空气(21% O2)、100% O2、卡波金(95% O2 + 5% CO2)、空气中2% CO2或空气中5% CO2。在使用室内空气、2% CO2或5% CO2通气时,呼吸暂停开始后观察到BOLD信号强度降低。在这些条件下,呼吸暂停期间PaO2和脑组织氧分压(PO2)降低。然而,卡波金通气时呼吸暂停诱导的BOLD信号强度不受影响,而100% O2通气时增加,在此期间PaO2保持恒定且脑组织PO2增加。当高碳酸血症期间基线CBF较高时,呼吸暂停诱导的BOLD信号下降更快。用2% CO2通气时,呼吸暂停诱导的CBF最大增加量为85±25%,而用室内空气通气时观察到增加44±8%。在其他通气条件下,呼吸暂停期间CBF观察到最小变化或无显著变化。这些结果表明,在不同生理条件下,BOLD信号变化与呼吸暂停反应中的组织PO2之间存在显著相关性。当PaO2保持恒定或变化极小时,呼吸暂停诱导的CBF增加会影响BOLD信号反应的幅度。

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