Brain oxygen, CO2, pH, and temperature monitoring: evaluation in the feline brain.
Brain oxygen, CO2, pH, and temperature monitoring: evaluation in the feline brain.
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DOI：
10.1227/00006123-199512000-00017
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发表时间：
1995-12
期刊：
影响因子：
4.8
通讯作者：
A. Zauner;R. Bullock;X. Di;H. Young
中科院分区：
文献类型：
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作者：
A. Zauner;R. Bullock;X. Di;H. Young
目前，还没有理想的方法来监测受伤的大脑。最近，一种简单、紧凑的光纤传感器已经可以用来测量血液中的氧气、二氧化碳、pH和温度。我们已经将这台仪器改装成在脑组织中连续使用，以测量氧分压、二氧化碳分压(PCO2)、pH和温度。为了评估这项新技术，我们在7只正常猫身上制造了高碳酸血症、低碳酸血症、颅内压升高和低氧血症。在另外六只动物中，传感器被放置在因阻塞左侧大脑中动脉而导致的局灶性脑缺血区。传感器读数与脑血流量测量、颅内压和脑组织学结果进行比较。还进行了一项体外实验，使用人血来测试传感器在广泛的二氧化碳分压和氧分压范围内的准确性。经过仔细的预校准和坚固的头骨固定，在6到8小时的实验中可以获得稳定的测量结果。在正常动物中，脑氧为42+/-9 mm Hg，脑二氧化碳为59+/-14 mm Hg，脑pH为7+/-0.2，脑温度为36.7+/-0.7℃。低碳酸血症和低氧血症使组织氧显著下降(OR=74+/-4 mm Hg；P<；0.001)。局灶性脑缺血导致脑氧含量迅速下降42%(25+/-7 mm Hg)，组织二氧化碳分压(PCO2)增加25%(71+/-23 mm Hg)。4小时后，在实验接近尾声时，脑氧进一步下降至19+/-6毫米汞。大脑中动脉闭塞后1h内局部脑血流量由基础值65+/-15ml/100g/min降至10+/-5ml/100g/min。然后在4小时的实验结束时逐渐增加到每100克每分钟15+/-5毫升。脑组织pH值与脑组织二氧化碳含量呈显著负相关。实验结束时，局灶性脑缺血组织的脑温从36.7±0.7摄氏度降至35.5±1.6摄氏度。体外实验表明，传感器读数与血气分析结果具有良好的线性相关性。使用单一传感器对受损或高危脑组织中的氧气、二氧化碳、pH和温度进行持续监测现在是可行的，因此可以改进对面临严重继发性脑损伤风险的神经外科患者的持续监测。
Currently, no ideal method exists for monitoring the injured brain. Recently, a single, compact, fiberoptic sensor has become available for measuring oxygen, CO2, pH and temperature in blood. We have adapted this instrument for continuous use in brain tissue to measure oxygen tension, carbon dioxide tension (pCO2), pH, and temperature. To evaluate this new technique, we produced hypercapnia, hypocapnia, intracranial pressure increase, and hypoxemia in seven normal cats. In an additional six animals, sensors were placed within a zone of focal brain ischemia induced by occluding the left middle cerebral artery. The sensor readings were compared with cerebral blood flow measurements, intracranial pressure, and brain histological findings. An in vitro experiment was also performed using human blood to test the accuracy of the sensor over a wide range of pCO2 and oxygen tension values. After careful precalibration and rigid cranium fixation, stable measurements could be obtained throughout the 6- to 8-hour experiments. In normal animals, brain oxygen was 42 +/- 9 mm Hg, brain CO2 was 59 +/- 14 mm Hg, brain pH was 7.0 +/- 0.2, and brain temperature was 36.7 +/- 0.7 degrees C. Hypocapnia and hypoxemia produced a significant decline in tissue oxygen ( or = 74 +/- 4 mm Hg; P < 0.001). Focal ischemia produced a rapid 42% decline in brain oxygen (25 +/- 7 mm Hg) and a 25% increase in tissue pCO2 (71 +/- 23 mm Hg). Brain oxygen further decreased to 19 +/- 6 mm Hg toward the end of the experiment, 4 hours later. After middle cerebral artery occlusion, the regional cerebral blood flow decreased to 10 +/- 5 ml per 100 g per minute, within the 1st hour, from a baseline value of 65 +/- 15 ml per 100 g per minute. It then gradually increased to 15 +/- 5 ml per 100 g per minute by the end of the 4-hour experiment. Brain pH was closely and inversely related to brain CO2. The brain temperature in the focally ischemic tissue decreased from 36.7 +/- 0.7 to 35.5 +/- 1.6 degrees C by the end of the experiment. The in vitro experiment demonstrated good linear correlation between the sensor readings and the blood gas analysis. Continuous monitoring of oxygen, CO2, pH, and temperature in damaged or at-risk brain tissue using a single sensor is now feasible and will, thus, allow improved continuous monitoring of neurosurgical patients who are at risk of significant secondary brain damage.