Manley G T, Pitts L H, Morabito D, Doyle C A, Gibson J, Gimbel M, Hopf H W, Knudson M M
School of Medicine, University of California San Francisco, Department of Neurological Surgery, San Francisco General Hospital, 94110, USA.
J Trauma. 1999 Feb;46(2):261-7. doi: 10.1097/00005373-199902000-00011.
Recently developed polarographic microelectrodes permit continuous, reliable monitoring of oxygen tension in brain tissue (PbrO2). The aim of this study was to investigate the feasibility and utility of directly monitoring PbrO2 in cerebral tissue during changes in oxygenation or ventilation and during hemorrhagic shock and resuscitation. We also sought to develop a model in which treatment protocols could be evaluated using PbrO2 as an end point.
Licox Clark-type polarographic probes were inserted in the brain tissue of 16 swine to monitor PbrO2. In eight swine, changes in PbrO2 were observed over a range of fractional concentrations of inspired O2 (FiO2) as well as during periods of hyperventilation and hypoventilation. In eight other swine, PbrO2 was monitored during a graded hemorrhage of up to 70% estimated blood volume and during the resuscitation period.
When FiO2 was elevated to 100%, PbrO2 increased from a baseline of 15+/-2 mm Hg to 36+/-11 mm Hg. Hyperventilation while breathing 100% oxygen resulted in a 40% decrease in PbrO2 (p < 0.05), whereas hypoventilation increased PbrO2 to 88 mm Hg (p < 0.01). A graded hemorrhage to 50% estimated blood volume significantly reduced PbrO2, mean arterial pressure, and intracranial pressure (p < 0.01). Continued hemorrhage to 70% estimated blood volume resulted in a PbrO2 of 2.9+/-1.5 mm Hg. After resuscitation, PbrO2 was significantly elevated, reaching 65+/-13 mm Hg (p < 0.01), whereas mean arterial pressure and cerebral perfusion pressure simply returned to baseline.
Directly measured PbrO2 was highly responsive to changes in FiO2, ventilatory rate, and blood volume in this experimental model. In particular, hypoventilation significantly increased PbrO2, whereas hyperventilation had the opposite effect. The postresuscitation increase in PbrO2 may reflect changes in both O2 delivery and O2 metabolism. These experiments set the stage for future investigations of a variety of resuscitation protocols in both normal and injured brain.
最近研发的极谱微电极能够持续、可靠地监测脑组织中的氧分压(PbrO2)。本研究的目的是探讨在氧合或通气变化期间以及失血性休克和复苏过程中直接监测脑组织中PbrO2的可行性和实用性。我们还试图建立一个模型,在该模型中可以使用PbrO2作为终点来评估治疗方案。
将Licox Clark型极谱探头插入16头猪的脑组织中以监测PbrO2。在8头猪中,观察了在一系列吸入氧分数(FiO2)范围内以及过度通气和通气不足期间PbrO2的变化。在另外8头猪中,在估计出血量高达血容量70%的分级出血过程中以及复苏期间监测PbrO2。
当FiO2升高到100%时,PbrO2从基线的15±2 mmHg增加到36±11 mmHg。在吸入100%氧气时进行过度通气导致PbrO2降低40%(p<0.05),而通气不足使PbrO2升高至88 mmHg(p<0.01)。分级出血至估计血容量的50%显著降低了PbrO2、平均动脉压和颅内压(p<0.01)。继续出血至估计血容量的70%导致PbrO2为2.9±1.5 mmHg。复苏后,PbrO2显著升高,达到65±13 mmHg(p<0.01),而平均动脉压和脑灌注压仅恢复到基线水平。
在该实验模型中,直接测量的PbrO2对FiO2、通气率和血容量的变化高度敏感。特别是,通气不足显著增加PbrO2,而过度通气则产生相反的效果。复苏后PbrO2的升高可能反映了氧输送和氧代谢的变化。这些实验为未来在正常和受伤大脑中对各种复苏方案的研究奠定了基础。