Wolf T, Lindauer U, Reuter U, Back T, Villringer A, Einhäupl K, Dirnagl U
Charité Hospital, Department of Neurology, Humboldt-University Berlin, Germany.
J Cereb Blood Flow Metab. 1997 Sep;17(9):950-4. doi: 10.1097/00004647-199709000-00004.
Intermittent peri-infarct depolarizations (PID), which spread from the vicinity of the infarction over the cortex, have been reported in focal ischemia. These depolarizations resemble cortical spreading depression except that they damage the cortex and enlarge the infarct volume possibly because of compromised oxygen delivery. The main purpose of this study was to evaluate the noninvasive technique of near-infrared spectroscopy (NIRS) for the identification of PID and to evaluate its capability for further pathophysiological studies. We used male barbiturate-anesthetized Wistar rats (n = 10) in which middle cerebral artery occlusion had been performed with a surgical thread. Middle cerebral artery occlusion resulted in a drop in parietally measured regional cerebral blood flow (laser Doppler flowmetry) to 31 +/- 8% of baseline flow. Six +/- 4 minutes after the induction of focal ischemia, 5 +/- 2 direct current deflections were recorded during a one-hour measurement period which may be regarded as PID. Measuring regional cerebral blood oxygenation changes with a NIRO 500 revealed dynamic concentration changes in the three chromophores oxyhemoglobin [HbO2], deoxyhemoglobin [Hb], and the oxidized form of cytochrome aa3 [CytO] during PID. Typically, an initial slight decrease of [HbO2] (-6.1 +/- 1.7 arbitrary units [AU] and an increase of [Hb] (+11.5 +/- 7.7 AU) were followed by an increase of [HbO2] (+10.8 +/- 4.7 AU) and a decrease of [Hb] (-4.7 +/- 5.5 AU); [CytO] decreased during the depolarizations (-2.0 +/- 1.2 AU). We conclude that NIRS can detect typical PID-associated changes in blood oxygenation. We hypothesize that during the course of PID, unlike "normal" spreading depression, hypoxygenation precedes hyperoxygenation of the microcirculation in a given cortex volume as the depolarization wave propagates through hemodynamically compromised to intact tissue. This would accord with the known damaging effect of PID. The NIRS "fingerprint" of PID encourages the search for PID during early stroke in patients.
间歇性梗死周围去极化（PID）从梗死灶附近扩散至整个皮层，在局灶性缺血中已有报道。这些去极化类似于皮层扩散性抑制，但不同的是它们会损伤皮层并扩大梗死体积，这可能是由于氧输送受损所致。本研究的主要目的是评估近红外光谱（NIRS）这种非侵入性技术用于识别PID的能力，并评估其在进一步病理生理学研究中的应用潜力。我们使用了10只经巴比妥类药物麻醉的雄性Wistar大鼠，通过手术线进行大脑中动脉闭塞。大脑中动脉闭塞导致顶叶区域脑血流（激光多普勒血流仪测量）降至基线血流的31±8%。局灶性缺血诱导后6±4分钟，在1小时的测量期内记录到5±2次直流偏转，可视为PID。使用NIRO 500测量局部脑血氧变化显示，在PID期间三种生色团氧合血红蛋白[HbO2]、脱氧血红蛋白[Hb]和细胞色素aa3的氧化形式[CytO]的浓度发生动态变化。典型的情况是，[HbO2]最初略有下降（-6.1±1.7任意单位[AU]），[Hb]升高（+11.5±7.7 AU），随后[HbO2]升高（+10.8±4.7 AU），[Hb]下降（-4.7±5.5 AU）；去极化期间[CytO]下降（-2.0±1.2 AU）。我们得出结论，NIRS可以检测到与PID相关的典型血氧变化。我们推测，在PID过程中，与“正常”的扩散性抑制不同，当去极化波通过血流动力学受损的组织传播至完整组织时，给定皮层体积内微循环的低氧状态先于高氧状态出现。这与已知的PID的损伤作用相符。PID的NIRS“指纹”特征促使我们在中风患者早期寻找PID。
