Severe controlled cortical impact in rats: Assessment of cerebral edema, blood flow, and contusion volume
Severe controlled cortical impact in rats: Assessment of cerebral edema, blood flow, and contusion volume
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DOI：
10.1089/neu.1995.12.1015
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发表时间：
1995-12-01
影响因子：
4.2
通讯作者：
DeKosky, ST
中科院分区：
文献类型：
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作者：
Kochanek, OM;Marion, DW;DeKosky, ST
受控皮质撞击(CCI)是一种当代的实验性脑挫伤模型。我们研究了严重CCI对大鼠的脑血管和神经病理影响。磁共振成像(MRI)在评估严重CCI后挫伤体积方面的应用也得到了证实。雄性SD大鼠58只，麻醉(异氟烷/N2O/O-2)，气管插管，机械通气，在左侧顶叶皮质造成重度CCI(深度3.0 mm，速度4m/s)。控制生理参数。分别于伤后2小时、24小时、48小时和7天观察脑水肿的变化[伤后2小时、24小时、48小时和7天脑组织水含量(%BW)]的变化。分别于2小时、24小时和7天进行局部脑血流量(ICBF)测定。第14天测量挫伤体积(组织学和图像分析测量)，并对6只大鼠进行MRI和组织学测量。重度CCI后存活率为96.2%。L-R的%BW差值在2 h为1.69+/-0.18%，24 h为3.00±0.08%，48 h为2.69+/-0.09%，7 d为0.94+/-0.21%。这些值均与对照组有差异(p<；0.05)。%BW在24 h和48 h大于2 h和7 d(p<；0.05)。与对照组相比，损伤侧大脑皮质(2和24 h)、皮质下白质(2和24 h)和海马区(2 H)LCBF显著降低(p<；0.05)。挫伤中心24 h的ICBF值为19.4+/-8.8mL100g(-1)min(-1)(p=0.011与正常对照)。大部分顶叶皮质和皮质下白质以及部分海马体和丘脑出现坏死。挫伤体积47.8+/-9.2 mm(3个)，占伤侧的14.4+/-2.1%。磁共振成像对挫伤体积的估计与组织学密切相关(r=0.941，p<；0.017)。大鼠严重CCI伴有挫伤、再生性水肿和明显的低灌注率，累及受损大脑半球的14%以上，死亡率最低。在该模型中，T-2加权MRI成功地、无创地识别了挫伤体积。
Controlled cortical impact (CCI) is a contemporary model of experimental cerebral contusion. We examined the cerebrovascular and neuropathologic effects of a severe CCI in rats. The utility of magnetic resonance imaging (MRI) for the assessment of contusion volume after severe CCI was also established. Severe CCI(3.0 mm depth, 4 m/sec velocity) to the left (L) parietal cortex was produced in anesthetized (isoflurane/N2O/O-2), intubated, and mechanically ventilated male Sprague-Dawley rats (n = 58). Physiologic parameters were controlled. The time coure of alterations in edema [L-R% brain water (% BW) in 3-mm coronal sections through injured and contralateral hemispheres, wet-dry weight] was evaluated at 2 h, 24 h, 48 h, and 7 days posttrauma. Local cerebral blood flow (ICBF, measured in 8 structures in each hemisphere by autoradiography) was evaluated at 2 h, 24 h, and 7 days. Contusion volume (measured by histology and image analysis) was assessed at 14 days and measured in 6 rats by both MRI and histology. The survival rate after severe CCI was 96.2%. The L-R difference in % BW increased to 1.69 +/- 0.18% at 2 h, 3.00 +/- 0.08% at 24 h, 2.69 +/- 0.09% at 48 h, and 0.94 +/- 0.21% at 7 days. These values all differed from the control (p < 0.05). The % BW was greater at 24 h and 48 h than at 2 h and 7 days (p < 0.05). Marked reductions in lCBF were limited to structures in the injured hemisphere and were observed in the parietal cortex (2 and 24 h), subcortical white matter (2 and 24 h), and hippocampus (2 h), (p < 0.05) vs control rats. In the contusion core, ICBF was 19.4 +/- 8.8 mL 100 g(-1) min(-1) at 24 h (p = 0.011 vs normal). Necrosis was seen in large portions of the parietal cortex and subcortical white matter, and portions of the hippocampus and thalamus. Contusion volume was 47.8 +/- 9.2 mm(3), which represented 14.4 +/- 2.1% of the traumatized hemisphere. Estimates of contusion volume by MRI and histology were closely correlated (r = 0.941, p < 0.017). Severe CCI in rats is accompanied by contusion, reproducible edema, and marked hypoperfusion, involving over 14% of the injured hemisphere, and can be produced with minimal mortality. T-2-weighted MRI successfully and noninvasively identifies contusion volume in this model.