开颅手术中动脉CO2分压和七氟烷对毛细血管静脉脑血流和氧饱和度的影响

背景手术中常规监测脑血流和氧饱和度是一项技术上的挑战。基于脑血管对CO，反应性的生理学原理．我们对新近开发的一种神经监测仪（oxygen—to—see，O2CTM）在开颅手术患者同步监测毛细血管静脉局部脑血流量（rvCBF）、血流速度（rvVelo）、氧饱和度（srvO2）和血红蛋白计数（rvHb）方面的表现进行评估。方法26例实施神经外科手术的患者，随机分g4采用呼气术浓度为1．4％和2．O％七氟烷进行麻醉。在颅骨切开后，在邻近手术部位肉眼所视正常的脑组织表面放置一光纤探头。每例患者同步监测较低动脉二氧化碳分压（PaCO2=35mmHg）和较高二氧化碳分压（PaC0，=45mmHg）时（随机排序）脑深度2mm和8mm处的组织脑血流。联合应用激光多普勒血流监测仪（rVcBF，rvVdo）和分光光度计（srvO，，rvHb）进行测量。采用线性模型检验较低和较高PaCO2、1.4％和2，0％呼气末七氟炕浓度2mm和8mm脑深度时rvCBF、rvVelo、srvO，和rvHb数值变化的线性关系。结果在脑组织深度2mm和8mm处，rvCBF和rvVelo随PaCO2升高而增加，与七氟皖浓度无关（P〈Q001）。高PaCO2使平均srvO2由50％升高至68％（P〈0．001）。与脑深度2mm处相比，脑深度8mm处的rvVelo（P〈0．001）和srvO，（P=0．007）较高。RvHb不受PaCO2变化的影响，但是与七氟垸浓度呈正相关（P=0．005）。结论PaCO：导致rvCBF和rvVelo增加，表明在呼气末七氟皖浓度1．4％和2％麻醉下，CO2增多可引起保护性血管扩张。SrvO2的连续升高表明PaCO2增高可导致脑动脉-静脉氧差缩小。RvHb不变表示测量期间未发生血液丢失。本研究显示，该神经监测仪可监测脑微血管主要静脉在不同PaCO2水平脑血流和氧饱和度的局部变化。

BACI（GROUND： Intraoperative routine monitoring of cerebral blood flow and oxygenation remains a tech- nological challenge. Using the physiological principle of carbon dioxide reactivity of cerebral vasculature, we investigated a re- cendy developed neuromonitoring device （oxygen-to-see, O2C. device） for simultaneous measurements of regional cerebral blood flow （rvCBF）, blood flow velocity （rvVelo）, oxygen saturation （srvO2）, and hemoglobin amount （rvHb） at the capillau venous level in patients subjected to craniotomy. METHODS： Twenty-six neurosurgical patients were randomly assigned to anesthesia with 1.4% or 2.0% sevoflurane end-tidal concentration. After craniotomy, a fiberoptic probe was applied on a macroscopically heal surface of cerebral tissue next to the site of surgery. Simultaneous measurements in 2 and 8 mm cere- bral depth were performed in each patient during lower （35 mm Hg） and higher （45 mm Hg） levels （random order） of arwrial carbon dioxide partial pressure （Paco2）. The principle of these measurements relies on the combination of laser-Doppler flowmetry （rvCBF, rvVelo） and photo-spectrometry （srvO2, rvHb）. Linear models were fitted to test changes of end points （rvCBF, rvVelo, srvO2, rvHb） in response to lower and higher levels of Paco2, 1.4% and 2.0% sevoflurane end-tidal concen- tration, and 2 and 8 mm cerebral depth. RESULTS： RvCBF and rvVelo were elevated by Paco2 independent of sevoflurane concentration in 2 and 8 mm depth of cerebral tissue （P 〈 0. 001 ）. Higher Paco2 induced an increase in mean srvO2 from 50% to 68% （P 〈 0. 001）. RvVelo （P 〈 0. 001） and srvO2 （P = 0. 007） were higher in 8 compared with 2 mm cerebral depth. RvHb was not influenced by alterations in Paco2 but positively correlated to sevoflurane concentration （P 〈 0. 005 ）. CONCLUSIONS： Increases in rvCl3F and rvVelo by Paco2 suggest preserved hypercapnic vasodilation under anesthesia with sevoflurane 1. 4% and 2.0% end-tidal concentration. A consecutive increase in srvO2 implies that cerebral arteriovenous difference in oxygen was decreased by elevated Paco2. Unchanged levels of rvHb signify that there was no blood loss duringmeasurements. Data suggest that the device allows detection of local changes in blood flow and oxygen saturation in response to different Paco2 levels in predominant venous cerebral microvessels.