Fitzpatrick J H, Gilboe D D
Isr J Med Sci. 1982 Jan;18(1):67-73.
Isolated brains were perfused for 30 min at 10, 20, 30 or 40 torr followed by up to 45 min of reoxygenation. Arterial and venous blood samples were drawn at frequent intervals before, during and after hypoxia for determination of oxygen and glucose content. Brain samples were frozen in situ before hypoxia, following 30 min of hypoxia and after 45 min of reoxygenation for measurement of adenine nucleotide and creatine phosphate (CrP) content. Neither the cerebral metabolic rate for oxygen (CMRO2) nor the ATP level returned to normal in the arterial pO2 10 and 20 torr groups. Although ATP reached normal levels in the arterial pO2 30 torr group following 45 min of reoxygenation. CMRO2 was 84% of normal and the CrP was only 63% of normal. However, ATP, CMRO2 and CrP were all normal in the arterial pO2 40 torr group following 45 min of reoxygenation. The failure of the arterial pO2 30 torr group to reach a normal CrP level is thought to be the result of a defect in brain energy metabolism whereby the cell was unable to generate ATP at a rate sufficient to restore CrP to normal levels. The defect appears to be signaled by a lower than normal CMRO2. The ability to effectively utilize oxygen to form ATP is believed to reside in the intact mitochondria of undamaged brain cells. Thus, the posthypoxic CMRO2 is an index of mitochondrial function and by implication it is a measure of the integrity of cerebral neurons.
分离的大脑在10、20、30或40托的压力下灌注30分钟，随后进行长达45分钟的复氧。在缺氧前、缺氧期间和缺氧后，每隔一段时间采集动脉和静脉血样，以测定氧气和葡萄糖含量。在缺氧前、缺氧30分钟后和复氧45分钟后，将脑样本原位冷冻，以测量腺嘌呤核苷酸和磷酸肌酸（CrP）含量。在动脉血氧分压为10和20托的组中，脑氧代谢率（CMRO2）和ATP水平均未恢复正常。尽管在复氧45分钟后，动脉血氧分压为30托的组中ATP达到了正常水平，但CMRO2仅为正常水平的84%，CrP仅为正常水平的63%。然而，在复氧45分钟后，动脉血氧分压为40托的组中，ATP、CMRO2和CrP均正常。动脉血氧分压为30托的组未能达到正常CrP水平，被认为是脑能量代谢缺陷的结果，即细胞无法以足以将CrP恢复到正常水平的速率产生ATP。这种缺陷似乎由低于正常水平的CMRO2所预示。有效利用氧气形成ATP的能力被认为存在于未受损脑细胞的完整线粒体中。因此，缺氧后的CMRO2是线粒体功能的一个指标，意味着它是衡量脑神经元完整性的一个指标。
