title: Interrelations of laser doppler flowmetry and brain tissue oxygen pressure during ischemia and reperfusion induced by an experimental mass lesion.
abstract: The objective of this study was to assess interrelations between bilateral changes of cortical laser doppler flowmetry and intraparenchymal, subcortical partial tissue oxygen tension in the course of an experimental trauma. Ten animals served as a sham group, 8 Sprague-Dawley rats received an unilateral, focal parietal mass lesion. The bilateral course of cortical blood flow measured by laser doppler flowmetry (LDF) was correlated with subcortical, intraparenchymal partial tissue oxygen tension [p(ti)O2]. In the sham-operated group, laser doppler mean flow values drifted between 9.0% and 9.5% and showed no significant changes over time neither between the hemispheres nor within each hemisphere. Absolute mean p(ti)O2 in sham-operated animals was 32.4 mm Hg in the left and 30.5 mm Hg in the right hemisphere. In the trauma group, mean laser doppler flow values during maximum brain compression decreased ipsilateral to 20.3% and contralateral to 34.4% of the baseline values. P(ti)O2 decreased ipsilateral from 25.9 to 6.6 mm Hg (25.4%) and contralateral from 22.6 to 9.8 mm Hg (43.6%). After balloon deflation, cortical LDF was restored much faster compared to p(ti)O2, but did not reach baseline values [ipsilateral 61.6% (p < 0.05); contralateral 75.8% of baseline values]. The p(ti)O2 values reached 25.2 mm Hg (97%) ipsilateral and 23.7 mm Hg (105%) contralateral. A temporary phase of reactive hyperemia occurred sporadically shortly after decompression. Both parameters showed a significant but rather weak correlation (r = 0.56; p < 0.001). Based upon these findings, we conclude that intraparenchymal, subcortical p(ti)O2 measurements supplemented on-line cortical CBF monitoring and score out discontinuous alternative measurement techniques in detecting hemodynamically relevant events. The small spatial resolution of LDF and p(ti)O2 probes, however, which in the small animal model may be of negligible influence, does raise the question whether the values obtained represent the microcirculatory situation of the human brain.
authors.affiliation: Department of Neurological Surgery, University of Würzberg, Germany. RBurger@t-online.de
authors.forename: R
authors.initials: R
authors.lastname: Burger
authors.forename: G H
authors.initials: GH
authors.lastname: Vince
authors.forename: J
authors.initials: J
authors.lastname: Meixensberger
authors.forename: M
authors.initials: M
authors.lastname: Bendszus
authors.forename: K
authors.initials: K
authors.lastname: Roosen
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications* / Q000209:etiology; D002404:Catheterization; D002540:Cerebral Cortex / Q000098:blood supply; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000503:physiopathology*; D017078:Laser-Doppler Flowmetry; D010100:Oxygen / Q000378:metabolism*; D010313:Partial Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow; D015427:Reperfusion Injury / Q000503:physiopathology*
chemical_list: D010100:Oxygen