Lewelt W, Jenkins L W, Miller J D
J Neurosurg. 1982 Mar;56(3):332-8. doi: 10.3171/jns.1982.56.3.0332.
To test the hypothesis that concussive brain injury interferes with the normal vasodilator response of the cerebral circulation to hypoxemia, 30 cats were subjected to mild (PaO2 50 mm Hg) and severe (PaO2 30 mm Hg) hypoxemia while measurements were made of arterial and intracranial pressure, regional cerebral blood flow (CBF), and arterial blood gases. Ten cats served as controls, 10 were subjected to mild fluid-percussion injury of the brain (0.8 to 1.7 atmospheres (atm)), and 10 to severe injury (2.4 to 4.1 atm). The CBF response to hypercapnia (PaCO2 50 mm Hg) was also tested in most animals, and the response of CBF autoregulation to hemorrhagic hypotension was tested in four animals of each group. Trauma was found to severely attenuate the capacity of CBF to increase during hypoxemia. Responsiveness to hypoxemia appeared to be better preserved in traumatized animals than was autoregulation, but was less robust than the response to hypercapnia.
为了验证脑震荡性损伤会干扰脑循环对低氧血症的正常血管舒张反应这一假说,对30只猫进行了轻度(动脉血氧分压50 mmHg)和重度(动脉血氧分压30 mmHg)低氧血症实验,同时测量动脉压、颅内压、局部脑血流量(CBF)和动脉血气。10只猫作为对照组,10只接受轻度脑流体冲击伤(0.8至1.7个大气压(atm)),10只接受重度损伤(2.4至4.1 atm)。在大多数动物中还测试了脑血流量对高碳酸血症(动脉血二氧化碳分压50 mmHg)的反应,并在每组的4只动物中测试了脑血流量自身调节对出血性低血压的反应。结果发现,创伤会严重削弱低氧血症期间脑血流量增加的能力。创伤动物对低氧血症的反应性似乎比自身调节更好地得以保留,但不如对高碳酸血症的反应强烈。