Evaluation of focal cerebral ischemia by NMR and histochemistry.

采用核磁共振（NMR）和免疫组织化学方法观察神经保护药物对动物脑缺血的影响。1）采用血管内闭塞法建立自发性高血压大鼠（STIR）局灶性脑缺血模型。然后，通过^1H NMR光谱检测受损区域中产生的乳酸。短暂性脑缺血时乳酸的升高幅度大于永久性脑缺血时。α-苯基-N-叔丁基硝酮（PBN）可抑制短暂性脑缺血时乳酸的升高。2）观察大脑中动脉阻塞30 min诱导的短暂性局灶性脑缺血后脑组织中白细胞介素-1受体拮抗剂（IL-1 ra）的表达。IL-1 ra表达于术后1d的神经元损伤边缘，术后4d增强，术后7 d消失。3）PBN和黄嘌呤氧化酶抑制剂oxypurinol对沙土鼠全脑缺血的神经保护作用。通过组织化学分析（甲酚紫染色）评价3.5 mm双侧颈动脉闭塞后一周的缺血性神经元损伤。缺血30 min后给予PBN可部分减轻神经元损伤，而给予oxypurinol则无此作用，表明NMR和免疫组化分析可准确评价药物对局灶性脑缺血的作用。

Effects of neroprotective drugs on cerebral ischemia were evaluated in animals using nuclear magnetic resonance (NMR) and immunohistochemical analyses.1) Focal cerebral ischemia was introduced in spontaneously hypertensive rats (STIR) using a method of intraluminal vascular occlusion. Then, lactate produced in the damaged area was detected by ^1H NMR.spectroscopy. The increase in lactate was larger in transient ischemia than that in permanent one. The increase in lactate in transient ischemia was attenuated by alpha-phenyl-N-tert- butyl nitrone (PBN), a superoxide scavenger.2) Expression of interleukin-1 receptor antagonist (IL- lra) was investigated in rat brain following transient focal cerebral ischemia induced by 30 min of middle cerebral artery occlusion. The expression of IL-lra was observed on the margin of the neuronal damage 1 day after operation, which was enhanced 4 days after operation and withdrawn 7 days after operation.3) Neuroprotective effects of PBN and oxypurinol, a xanthine oxidase inhibitor, were examined in gerbil global brain .ischemia. Ischemic neuronal damage were evaluated one week after a 3.5 mm bilateral carotid artery occlusion by a histochemical analysis (cresyl violet staining). PBN administered 30 min after ischemia partially attenuated the neuronal damage, while oxypurinol did not.These results indicated that the drug effects on focal cerebral ischemia were precisely evaluated using NMR and immunohistochemical analyses.