Brain tissue acid-base response to hypercapnia in neurosurgical patients.
Brain tissue acid-base response to hypercapnia in neurosurgical patients.
复制标题
神经外科患者脑组织对高碳酸血症的酸碱反应。
DOI：
10.1080/01616412.1995.11740354
复制
发表时间：
1995
影响因子：
1.9
通讯作者：
J. Ausman
中科院分区：
文献类型：
--
作者：
W. Hoffman;F. Charbel;G. Edelman;J. Ausman
这些研究在神经外科患者中进行，以确定高碳酸血症期间脑组织对pH值变化的非碳酸氢盐缓冲。开颅手术后，将一个连续测量氧气压力、二氧化碳压力、pH值和温度的传感器插入9名受试者的皮质组织中。根据Henderson-Hasselbach方程计算Bicycline浓度。基线测量后，PaCO 2升高10 mmHg，持续10分钟。组织pCO 2升高9 mmHg（p < 0.05），组织pO 2无变化。在6名患者中，组织碳酸氢盐浓度从18 meq L-1增加到20 meq L-1（p < 0.05），表明非碳酸氢盐缓冲机制使氢离子（H+）的增加衰减了40-50%。3例患者在高碳酸血症期间未显示组织碳酸氢盐增加; 2例患者的基线组织pH值低于6.5，1例患者在CO2激发期间显示组织缺氧体征。在所有患者中，高碳酸血症期间组织H+的增加与基线组织碳酸氢盐浓度相关。当基线碳酸氢盐降低至10 meq L-1以下时，观察到H+显著增加。这些结果表明，当组织碳酸氢盐耗尽时，高碳酸血症期间H+诱导损伤的风险增加。
These studies were conducted in neurosurgical patients to determine brain tissue nonbicarbonate buffering of pH changes during hypercapnia. Following a craniotomy, a sensor which continuously measures oxygen pressure, carbon dioxide pressure, pH and temperature was inserted into cortex tissue of nine subjects. Bicarbonate concentration was calculated from the Henderson-Hasselbach equation. Following baseline measures, PaCO2 was increased 10mmHg for 10 min. Tissue pCO2 increased 9 mmHg (p < 0.05) without a change in tissue pO2. In six patients, tissue bicarbonate concentration increased from 18 to 20 meq L-1 (p < 0.05), indicating a 40-50% attenuation of the increase in hydrogen ion (H+) by nonbicarbonate buffering mechanisms. Three patients showed no increase in tissue bicarbonate during hypercapnia; 2 had baseline tissue pH less than 6.5 and one displayed signs of tissue hypoxia during the CO2 challenge. In all patients, increases in tissue H+ during hypercapnia were related to baseline tissue bicarbonate concentration. Marked increases in H+ were seen when baseline bicarbonate decreased below 10 meq L-1. These results suggest that when tissue bicarbonate is depleted, the risk of H+ induced injury during hypercapnia is increased.