Brain nitric oxide changes after controlled cortical impact injury in rats

Brain nitric oxide changes after controlled cortical impact injury in rats
复制标题

DOI:
10.1152/jn.2000.83.4.2171
复制
发表时间:
2000-04-01
影响因子:
2.5
通讯作者:
Robertson, CS
Robertson, CS
中科院分区:
医学3区
文献类型:
--
作者:
Cherian, L;Goodman, JC;Robertson, CS

文献摘要

被引文献

相似文献

在大鼠进行5米/秒、3毫米变形控制的皮质撞击损伤后,在撞击部位测量了一氧化氮(NO)以及NO的终产物硝酸盐和亚硝酸盐。撞击损伤后立即(且如果NO和微透析探针可以更换的话),NO浓度从基线水平升高了83 ± 16(标准误)纳摩尔,而假损伤动物仅为0.5 ± 4纳摩尔(P < 0.001)。这种NO的显著升高发生在损伤引起血压(BP)和颅内压(ICP)初始升高时。在血压和颅内压初始升高之后,血压下降并稳定在比损伤前值低约20毫米汞柱的值,颅内压稳定在平均值20毫米汞柱,而假损伤动物为8毫米汞柱。这使得平均脑灌注压为40 - 50毫米汞柱,而假损伤动物为65 - 75毫米汞柱。在3小时监测期的剩余时间里,这些值相对恒定。在此期间NO值也趋于稳定。撞击损伤后1小时,使用NO电极直接测量的NO浓度从基线值平均下降了25 ± 6纳摩尔,在3小时监测期的剩余时间里,NO浓度始终显著低于基线值。损伤后20 - 30分钟,透析液中硝酸盐/亚硝酸盐的浓度也平均下降了341 ± 283纳摩尔。在3小时监测期的剩余时间里,透析液中亚硝酸盐/硝酸盐浓度始终低于损伤前基线值。损伤前用L - 硝基 - 精氨酸甲酯(L - NAME)处理减弱了损伤引起的NO升高,并导致损伤后1小时更严重的即时颅内高压和更严重的全身性低血压。用L - NAME预处理的死亡率也为67%,而未处理的动物为1%。
Nitric oxide (NO) and the NO end products, nitrate and nitrite, were measured at the impact site after a 5-m/s, 3-mm deformation controlled cortical impact injury in rats. Immediately after the impact injury and the NO and microdialysis probes could be replaced, there was an increase from baseline in NO concentration of 83 +/- 16 (SE) nM, compared with 0.5 +/- 4 nM in the sham injured animals (P < 0.001). This marked increase in NO occurred at the time of the initial rise in blood pressure (BP) and intracranial pressure (ICP) in response to the injury. After the initial increase in BP and ICP, the BP decreased and stabilized at a value which was similar to 20 mmHg below the preinjury values, and ICP plateaued at an average value of 20 mmHg, compared with 8 mmHg in the sham-injured animals. This provided an average cerebral perfusion pressure of 40-50 mmHg, compared with 65-75 mmHg fur the sham-injured animals. These values were relatively constant for the remainder of the 3-h monitoring period. The NO values also stabilized during this time period. By 1 h after the impact injury the NO concentration measured directly using the NO electrode had decreased from baseline values by an average value of 25 +/- 6 nM, NO concentration remained significantly lower than baseline values throughout the remainder of the 3-h monitoring period. The concentration of nitrate/nitrite in the dialysate fluid also decreased by an average value of 341 +/- 283 nM 20-30 min after the injury. Dialysate nitrite/nitrate concentrations remained less than the preinjury baseline values throughout the remainder of the 3-h monitoring period. Preinjury treatment with L-nitro-arginine methyl ester (L-NAME) blunted the injury-induced increase in NO and resulted in more severe immediate intracranial hypertension and more severe systemic hypotension at one hour after injury. Mortality was also 67% with L-NAME pretreatment, compared with 1% in untreated animals.