Tenny R T, Sharbrough F W, Anderson R E, Sundt T M
Ann Neurol. 1980 Dec;8(6):564-73. doi: 10.1002/ana.410080604.
Epileptogenic foci were created by topical application of penicillin to the cerebral cortex in 40 paralyzed and artificially ventilated cats receiving halothane anesthesia. The animals were divided into two equal groups to compare primary and secondary foci. The following variables were recorded at normocapnia, hypocapnia, and hypercapnia prior to and during seizure activity: cerebral blood flow (CBF), determined by clearance of xenon 133; cortical redox states, measured by the fluorescence of reduced pyridine nucleotides (PN); brain pH, measured using a lipid-soluble, pH-sensitive fluorescent indicator; and electroencephalograms (EEG). Mean arterial blood pressure, arterial pH, arterial carbon dioxide tension (PaCO2), and arterial oxygen tension (PaO2) were monitored in each animal. All animals had a normal PaCO2-CBF response prior to the creation of a seizure focus, assuring the presence of autoregulation and normal metabolic function. CBF increased equally with seizures in the primary and secondary hemispheres. The relative increase was related to the PaCO2 but approximated 68% at normocapnia. There was an alteration in the PaCO2-CBF response with seizures, but the ability of the cerebral vasculature to constrict and dilate with hypocapnia and hypercapnia was retained. There was no significant difference in the reduced PN signal with variations in PaCO2 prior to seizures, but there was an apparent 10 to 15% fall with seizures. The "equivalent" intracellular pH fell to 6.94 at normocapnia in the primary focus but remained essentially unchanged from the control value of 7.10 in the secondary focus. These differences in pH were consistent with the greater degree of seizure activity observed in the primary focus. We conclude that a nonhypoxic acidosis existed in the primary focus and that changes in CBF were not related to it because the CBF changed equally in both hemispheres.
在40只接受氟烷麻醉、瘫痪并进行人工通气的猫中,通过将青霉素局部应用于大脑皮层来产生致痫灶。将动物分成两组,每组数量相等,以比较原发性和继发性病灶。在发作活动之前和期间,于正常碳酸血症、低碳酸血症和高碳酸血症状态下记录以下变量:通过氙133清除率测定的脑血流量(CBF);通过还原吡啶核苷酸(PN)荧光测量的皮层氧化还原状态;使用脂溶性、pH敏感荧光指示剂测量的脑pH值;以及脑电图(EEG)。监测每只动物的平均动脉血压、动脉pH值、动脉二氧化碳分压(PaCO2)和动脉氧分压(PaO2)。在致痫灶形成之前,所有动物的PaCO2-CBF反应均正常,确保了自动调节和正常代谢功能的存在。原发性和继发性半球的CBF在发作时均同等增加。相对增加与PaCO2相关,但在正常碳酸血症时约为68%。发作时PaCO2-CBF反应发生改变,但脑血管在低碳酸血症和高碳酸血症时收缩和扩张的能力得以保留。发作前PaCO2变化时,还原PN信号无显著差异,但发作时明显下降10%至15%。在正常碳酸血症时,原发性病灶的“等效”细胞内pH值降至6.94,但继发性病灶的该值与对照值7.10基本保持不变。这些pH值差异与原发性病灶中观察到的更强发作活动程度一致。我们得出结论,原发性病灶中存在非低氧性酸中毒,且CBF变化与之无关,因为两个半球的CBF变化相同。