Zhang F, Iadecola C
Department of Neurology, University of Minnesota, Minneapolis 55455.
Neuroreport. 1993 May;4(5):559-62. doi: 10.1097/00001756-199305000-00024.
We used the nitric oxide (NO) donor sodium nitroprusside (SNP) and the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME) to study the role of NO in the ischemic damage produced by occlusion of the rat middle cerebral artery (MCA). After MCA occlusion, intracarotid administration of SNP (2.5 mg kg h-2 for 1 h) enhanced the recovery of neocortical cerebral blood flow and of the EEG and reduced cortical infarct size by 76 +/- 2% (p < 0.01; n = 5). In contrast, administration of L-NAME (10 mg kg h-2) worsened the recovery of CBF and EEG and increased infarct size (+ 60 +/- 16%; p < 0.05; n = 5). The findings indicate that NO improves blood flow and reduces tissue damage after focal cerebral ischemia. Thus, NO donors could have an important role in the management of acute ischemic stroke.
我们使用一氧化氮(NO)供体硝普钠(SNP)和NO合酶抑制剂L-硝基精氨酸甲酯(L-NAME)来研究NO在大鼠大脑中动脉(MCA)闭塞所致缺血性损伤中的作用。MCA闭塞后,经颈内动脉给予SNP(2.5 mg·kg·h⁻²,持续1小时)可增强新皮质脑血流和脑电图的恢复,并使皮质梗死面积减少76±2%(p<0.01;n=5)。相比之下,给予L-NAME(10 mg·kg·h⁻²)会使脑血流和脑电图的恢复恶化,并增加梗死面积(+60±16%;p<0.05;n=5)。这些发现表明,NO可改善局灶性脑缺血后的血流并减少组织损伤。因此,NO供体在急性缺血性卒中的治疗中可能具有重要作用。