Hyperbaric oxygen therapy for reduction of secondary brain damage in head injury: An animal model of brain contusion
Hyperbaric oxygen therapy for reduction of secondary brain damage in head injury: An animal model of brain contusion
复制标题
DOI：
10.1089/089771504772695931
复制
发表时间：
2004-01-01
影响因子：
4.2
通讯作者：
Soustiel, JF
中科院分区：
文献类型：
--
作者：
Palzur, E;Vlodavsky, E;Soustiel, JF
脑挫伤是最常见的外伤性病变之一，也是最常见的二次手术减压指征。本研究的目的是探讨病灶周围继发性脑损伤的生理学，并评估高压氧治疗（HBOT）在治疗这些病变中的价值。将5只Sprague-Dawley大鼠分为5组，每组5只进行皮质负压诱导的动态皮质变形实验。DCD在真空部位产生的脑损伤被证明是可重复的。研究方案包括：(1)单独DCD， (2) DCD和HBOT， (3) DCD和术后缺氧和HBOT， (4) DCD，术后缺氧和HBOT， (5) DCD和常压高氧。4天后处死动物。组织切片显示损伤部位皮质局部大体组织丢失，并伴有出血。在所有病例中，通过计算每0.5 mm厚的连续病变周围层中末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）和caspase 3阳性细胞的数量来评估继发性脑损伤的严重程度。第1组（12.24%）淋巴结周围TUNEL阳性细胞提示凋亡参与。术后缺氧显著提高了这些指标（31.75%,p < 0.001）。HBOT显著降低了各层TUNEL阳性细胞数量和病变体积所表达的继发脑损伤的严重程度和程度（第2组和第4组第1层TUNEL阳性细胞分别占4.7%和9%，p < 0.0001和p < 0.003）。常压高氧也被证明是有益的，尽管程度较小。本研究证明真空脑损伤模型是一种可重复性的脑挫伤模型。目前的研究结果还表明，HBOT可能会限制脑挫伤的发展，并证明进一步的实验研究是合理的。
Cerebral contusions are one the most frequent traumatic lesions and the most common indication for secondary surgical decompression. The purpose of this study was to investigate the physiology of perilesional secondary brain damage and evaluate the value of hyperbaric oxygen therapy (HBOT) in the treatment of these lesions. Five groups of five Sprague-Dawley rats each were submitted to dynamic cortical deformation (DCD) induced by negative pressure applied to the cortex. Cerebral lesions produced by DCD at the vacuum site proved to be reproducible. The study protocol entailed the following: (1) DCD alone, (2) DCD and HBOT, (3) DCD and post-operative hypoxia and HBOT, (4) DCD, post-operative hypoxia and HBOT, and (5) DCD and normobaric hyperoxia. Animals were sacrificed after 4 days. Histological sections showed localized gross tissue loss in the cortex at injury site, along with hemorrhage. In all cases, the severity of secondary brain damage was assessed by counting the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 3-positive cells in successive perilesional layers, each 0.5 mm thick. Perilesional TUNEL positive cells suggested the involvement of apoptosis in group 1 (12.24% of positive cells in layer 1). These findings were significantly enhanced by post-operative hypoxia (31.75%, p < 0.001). HBOT significantly reduced the severity and extent of secondary brain damage expressed by the number of TUNEL positive cells in each layer and the volume of the lesion (4.7% and 9% of TUNEL positive cells in layer I in groups 2 and 4 respectively, p < 0.0001 and p < 0.003). Normobaric hyperoxia also proved to be beneficial although in a lesser extent. This study demonstrates that the vacuum model of brain injury is a reproducible model of cerebral contusion. The current findings also suggest that HBOT may limit the growth of cerebral contusions and justify further experimental studies.