Wolf T, Lindauer U, Villringer A, Dirnagl U
Department of Neurology, Charité Hospital, Humboldt University, Berlin, Germany.
Brain Res. 1997 Jul 4;761(2):290-9. doi: 10.1016/s0006-8993(97)00354-5.
We investigated the influence of hyperoxia (arterial pO2 446 +/- 43 mmHg) and hyperglycemia (blood glucose 19.4 mmol/l) on somatosensory stimulation (whisker deflection) employing laser Doppler flowmetry (LDF). Our aim was to test the hypothesis that a possible substrate-sensing mechanism for glucose and oxygen contributes to the coupling between cortical activity and regional cerebral blood flow (rCBF) in order to match increased demand with substrates. In addition, we looked at the influence of hyperglycemia (blood glucose 17.9 mmol/l) and hypercapnia (arterial pCO2 62 mmHg) on rCBF (LDF) and regional cerebral blood oxygenation changes (rCBO) in the even stronger metabolic stimulus of cortical spreading depression (CSD). For the latter we employed the new non-invasive technique of near infrared spectroscopy (NIRS). All experiments were done using chloralose/urethane-anesthetized rats. Somatosensory stimulation increased rCBF by about 20% of baseline, in the case of both norm- and hyperoxia as well as both normo- and hyperglycemia. The blood-flow response to CSD consisted of a temporary sharp increase in rCBF to more than 400%. At the same time, the concentration of oxyhemoglobin [HbO2] increased, while deoxyhemoglobin [Hb] decreased, indicating excessive oxygenation. Hyperglycemia altered neither the rCBF nor the rCBO response. Preexisting hypercapnia, however, produced reductions in both hyperperfusion (rCBF) and hyperoxygenation (rCBO) during CSD. We found that, for experimental hyperglycemia, i.v. may be superior to i.p. application of glucose because of the latter's side effects in connection with blood flow. Our findings cannot support the hypothesis of a substrate sensing mechanism in coupling.
我们采用激光多普勒血流仪（LDF）研究了高氧（动脉血氧分压446±43 mmHg）和高血糖（血糖19.4 mmol/l）对体感刺激（触须偏转）的影响。我们的目的是检验这样一个假设，即葡萄糖和氧气可能存在的底物感知机制有助于皮层活动与局部脑血流（rCBF）之间的耦合，以便使增加的需求与底物相匹配。此外，我们研究了高血糖（血糖17.9 mmol/l）和高碳酸血症（动脉血二氧化碳分压62 mmHg）对皮层扩散性抑制（CSD）这种更强代谢刺激下的rCBF（LDF）和局部脑血氧变化（rCBO）的影响。对于后者，我们采用了近红外光谱（NIRS）这种新的非侵入性技术。所有实验均使用水合氯醛/乌拉坦麻醉的大鼠进行。在常氧和高氧以及正常血糖和高血糖情况下，体感刺激均使rCBF增加约为基线的20%。对CSD的血流反应包括rCBF暂时急剧增加至超过400%。同时，氧合血红蛋白[HbO2]浓度增加，而脱氧血红蛋白[Hb]浓度降低，表明氧合过度。高血糖既未改变rCBF反应，也未改变rCBO反应。然而，预先存在的高碳酸血症在CSD期间导致高灌注（rCBF）和高氧合（rCBO）均降低。我们发现，对于实验性高血糖，静脉注射葡萄糖可能优于腹腔注射，因为腹腔注射葡萄糖会产生与血流相关的副作用。我们的研究结果不支持耦合中存在底物感知机制这一假设。
