Okeda R, Funata N, Song S J, Higashino F, Takano T, Yokoyama K
Acta Neuropathol. 1982;56(4):265-72. doi: 10.1007/BF00691257.
Since in a previous study hypoxia and subsequent hypotension were considered to be essential for the pathogenesis of carbon monoxide encephalopathy (CO-encephalopathy), experiments were conducted to see whether a combination of nitrogen hypoxia and subsequent systemic hypotension of similar degree and duration as in the previous experimental CO poisoning could induce the same lesion in the CNS of cats. The partial pressure of blood oxygen was reduced to less then 26 mm Hg by increasing the concentration of nitrogen in N2/O2 gas to be inhaled in 1.5h and then the aortic blood pressure (BP) was reduced to 60-80 mm Hg by blood depletion and ganglion-blockage for 1h. In 11 of the 15 cats, lesions were produced in the CNS which were similar by light and electron microscopy to those in CO-encephalopathy. In control groups which were treated by hypoxemia only, hypotension only or a combination CO2-gas inhalation and hypotension without hypoxemia, such lesions were not found in the cerebral white matter. Considering the pathogenesis of lesions in the cerebral white matter in both nitrogen hypoxia and CO-poisoning, two factors i.e., hypoxemia and subsequent systemic hypotension, are common and essential. Further, the enormous vasodilatation in the cerebral white matter induced by hypoxemia and subsequent drop in BP seem to cause a more severe circulatory disturbance in the cerebral white matter than in the cortex.
由于在先前的一项研究中,低氧血症及随后的低血压被认为是一氧化碳脑病(CO脑病)发病机制中的关键因素,因此开展了实验,以探究与先前实验性CO中毒中程度和持续时间相似的氮气低氧血症与随后的全身性低血压联合作用,是否会在猫的中枢神经系统中诱发相同的病变。通过在1.5小时内增加吸入的N2/O2气体中氮气的浓度,将血氧分压降至26 mmHg以下,然后通过放血和神经节阻滞使主动脉血压(BP)在1小时内降至60 - 80 mmHg。在15只猫中的11只中,中枢神经系统出现了病变,通过光镜和电镜观察,这些病变与CO脑病中的病变相似。在仅接受低氧血症、仅接受低血压或接受二氧化碳气体吸入与低血压联合但无低氧血症治疗的对照组中,脑白质未发现此类病变。考虑到氮气低氧血症和CO中毒时脑白质病变的发病机制,低氧血症和随后的全身性低血压这两个因素是共同且关键的。此外,低氧血症引起的脑白质巨大血管扩张以及随后的血压下降,似乎在脑白质中造成的循环障碍比在皮质中更严重。