Miller C L, Alexander K, Lampard D G, Brown W A, Griffiths R
Stroke. 1980 Sep-Oct;11(5):542-8. doi: 10.1161/01.str.11.5.542.
Following 5 minutes of global ischemia, local cerebral blood flow (LCBF) was shown to have an initial reactive hyperemia that was followed, within the first hour, by persistent hypoperfusion (Part I). Intracranial pressure (ICP) was never elevated during the period of poor reperfusion. These experiments attempted to reverse the state of subnormal LCBF by inducing hypercarbia or hyocarbia or maintaining normocarbia. Although hypocarbia did increase LCBF at several electrode sites, neither the intracerebral steal syndrome nor the "squeeze" syndrome are a dominant consequence of hypercarbia in this model of global ischemia. Hypercarbia was consistently more effective in elevating LCBFs and in recovery of the electrocorticogram. It appears that, in the absence of raised ICP, hypercarbia may be preferred to normal or low PACO2,. Even though hypercarbia was superior to normocarbia or hypocarbia, hypercarbia was not a completely satisfactory regimen for reversing the state of poor reperfusion.
在全脑缺血5分钟后,局部脑血流量(LCBF)显示出最初的反应性充血,在第一个小时内,随后出现持续性灌注不足(第一部分)。在再灌注不良期间,颅内压(ICP)从未升高。这些实验试图通过诱导高碳酸血症或低碳酸血症或维持正常碳酸血症来逆转LCBF低于正常的状态。尽管低碳酸血症在几个电极部位确实增加了LCBF,但在这种全脑缺血模型中,脑内盗血综合征和“挤压”综合征都不是高碳酸血症的主要后果。高碳酸血症在提高LCBF和恢复脑电图方面一直更有效。似乎在没有ICP升高的情况下,高碳酸血症可能比正常或低动脉血二氧化碳分压(PACO2)更可取。尽管高碳酸血症优于正常碳酸血症或低碳酸血症,但高碳酸血症并不是逆转再灌注不良状态的完全令人满意的方案。