Güney Onder, Erdi Fatih, Esen Hasan, Kiyici Aysel, Kocaogullar Yalcin
Department of Neurosurgery, Selcuk University Meram Faculty of Medicine, Konya, Turkey.
World Neurosurg. 2010 Jan;73(1):42-9; discussion e3. doi: 10.1016/j.surneu.2009.06.003. Epub 2009 Aug 7.
This study investigated the ability of NAC to prevent cerebral vasospasm in a rabbit model of SAH.
Twenty-one, male New Zealand white rabbits were randomly divided into 3 groups of 7 rabbits each: group 1 (control), group 2 (SAH only), group 3 (SAH + NAC treatment). NAC (150 mg/kg, single dose, IP) was administered just before SAH and continued until 72 hours after SAH in group 3. Animals were killed 72 hours after SAH. Tissue MDA levels, SOD, and GSH-Px activities were measured, and basilar artery cross-sectional areas, arterial wall thickness, and endothelial apoptosis in a cross section of basillary artery were determined in all groups.
Intraperitoneal administration of NAC was found to be markedly effective against developing a cerebral vasospasm following a SAH in rabbits. It could significantly reduce elevated lipid peroxidation and increase the level of tissue GSH-Px and SOD enzymatic activities. Also, NAC treatment was found to be effective in increasing the luminal area and reducing wall thickness of the basilar artery. The morphology of arteries in the NAC treatment group was well protected. NAC markedly reduced apoptotic index and protects the endothelial integrity.
This study demonstrates, for the first time, that NAC treatment attenuates cerebral vasospasm in a rabbit SAH model. NAC treatment has significant neuroprotective effect and markedly prevents cerebral vasospasm after SAH. In conclusion, the NAC treatment might be beneficial in preventing cerebral vasospasm after SAH, thus showing potential for clinical implications.
本研究在兔蛛网膜下腔出血(SAH)模型中探究了N-乙酰半胱氨酸(NAC)预防脑血管痉挛的能力。
21只雄性新西兰白兔被随机分为3组,每组7只:第1组(对照组)、第2组(仅SAH组)、第3组(SAH + NAC治疗组)。在SAH前即刻给予第3组NAC(150 mg/kg,单次剂量,腹腔注射),并持续至SAH后72小时。SAH后72小时处死动物。测量所有组的组织丙二醛(MDA)水平、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,并测定基底动脉横截面积、动脉壁厚度以及基底动脉横断面的内皮细胞凋亡情况。
发现腹腔注射NAC对兔SAH后发生脑血管痉挛具有显著疗效。它可显著降低升高的脂质过氧化水平,并提高组织GSH-Px水平和SOD酶活性。此外,发现NAC治疗可有效增加基底动脉的管腔面积并减小其壁厚。NAC治疗组动脉的形态得到良好保护。NAC显著降低凋亡指数并保护内皮细胞完整性。
本研究首次证明,NAC治疗可减轻兔SAH模型中的脑血管痉挛。NAC治疗具有显著的神经保护作用,并可显著预防SAH后的脑血管痉挛。总之,NAC治疗可能对预防SAH后的脑血管痉挛有益,因此具有临床应用潜力。