Department of Neurosurgery, Thomas Jefferson University, 1025 Walnut Street, Philadelphia, PA 19107, USA.
Brain Res. 2009 Dec 11;1305:183-91. doi: 10.1016/j.brainres.2009.09.104. Epub 2009 Oct 3.
Hypertonic saline is currently being used in the treatment of patients with post-traumatic cerebral edema and elevated intracranial pressure resulting from TBI. A limited number of studies show the cellular effects of hypertonic saline and no studies, to our knowledge, have investigated the effects on astrocytes. The role of astrocyte responses after traumatic brain injury remains unclear. There is evidence that reduced astrocyte proliferation is detrimental while increased hypertrophy and proliferation are signs of increased injury severity. Therefore, this study focused on the hypothesis that hypertonic saline-induced improvements in histological outcome are time dependent and may be associated with alterations in astrocyte hypertrophy after cortical contusion injury. Histopathological changes at 7 days after controlled cortical impact (CCI) injury were examined. Brain tissue loss determined using cresyl violet staining and astrocyte hypertrophy and proliferation were assessed using glial fibrillary acidic protein immunostaining in hypertonic saline and normal saline treated rats, and untreated, injured controls. Effects of the timing of hypertonic saline treatment administration on tissue loss were also examined. Plasma osmolarity and sodium levels were measured over 4 h and again at 24 h following hypertonic saline administration. Results show that hypertonic saline treatment reduced tissue loss that correlated with attenuated astrocyte hypertrophy characterized by reductions in astrocyte immunoreactivity without changes in the number of astrocytes after CCI injury. Delayed treatment of hypertonic saline resulted in the greatest reduction in tissue loss compared to all other treatments indicating that there is a therapeutic window for hypertonic saline use after traumatic brain injury.
高渗盐水目前被用于治疗创伤性脑损伤导致的外伤性脑水肿和颅内压升高的患者。少数研究表明了高渗盐水的细胞作用,据我们所知,尚无研究调查其对星形胶质细胞的影响。星形胶质细胞反应在创伤性脑损伤后的作用仍不清楚。有证据表明,星形胶质细胞增殖减少是有害的,而肥大和增殖增加则是损伤严重程度增加的标志。因此,本研究的假设是,高渗盐水诱导的组织学结果改善是时间依赖性的,并且可能与皮质挫伤损伤后星形胶质细胞肥大的改变有关。研究使用皮质撞击伤(CCI)损伤后 7 天检查组织学变化。使用 cresyl 紫染色确定脑组织丢失,使用胶质纤维酸性蛋白免疫染色评估高渗盐水和生理盐水处理大鼠以及未处理、受伤对照中的星形胶质细胞肥大和增殖。还研究了高渗盐水治疗给药时间对组织丢失的影响。在高渗盐水给药后 4 小时和 24 小时测量血浆渗透压和钠水平。结果表明,高渗盐水治疗减少了组织丢失,与 CCI 损伤后星形胶质细胞肥大减弱相关,其特征是星形胶质细胞免疫反应性降低,而星形胶质细胞数量无变化。与其他所有治疗相比,延迟高渗盐水治疗导致组织丢失的减少最大,这表明在创伤性脑损伤后使用高渗盐水存在治疗窗。