Differences in infarct evolution between lipopolysaccharide-induced tolerant and nontolerant conditions to focal cerebral ischemia
Differences in infarct evolution between lipopolysaccharide-induced tolerant and nontolerant conditions to focal cerebral ischemia
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DOI：
10.3171/jns.2005.103.4.0715
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发表时间：
2005-10-01
影响因子：
4.1
通讯作者：
Kirino, T
中科院分区：
文献类型：
--
作者：
Furuya, K;Zhu, LD;Kirino, T
Object.虽然脑组织可能会受到保护，以前的预处理，在局灶性脑缺血过程中，在这种预处理的脑组织梗死的时间演变在很大程度上是未知的。因此，在这项研究中，作者从事长期的观察与磁共振（MR）成像，以澄清的差异，病变演变之间的耐受和不耐受的条件。静脉注射细菌脂多糖（LPS; 0.9 mg/kg）以诱导交叉缺血耐受。72小时后，在自发性高血压大鼠中诱导局灶性脑缺血。采用7.05T磁共振仪，于缺血后6 h、24 h、4d、7 d、14 d进行脑MRI扫描，LPS组在缺血后6 h有明显的脑损伤减轻作用。用LPS预处理不仅延迟而且通过减小损伤尺寸防止缺血性细胞死亡。病变缩小是缺血后14天内观察到的持续效应。LPS组梗死周边区局部脑血流量（ICBF）的减少明显受到抑制，这与内皮型一氧化氮合酶（eNOS）的表达有关。显著保存ICBF在梗死周围区域，这是相关的eNOS的持续上调，可能是一个候选人的长期抑制作用，在LPS诱导的耐受状态的梗死演变。
Object. Although brain tissue may be protected by previous preconditioning, the temporal evolution of infarcts in such preconditioned brain tissue during focal cerebral ischemia is largely unknown. Therefore, in this study the authors engaged in long-term observation with magnetic resonance (MR) imaging to clarify the difference in lesion evolution between tolerant and nontolerant conditions.Methods. Bacterial lipopolysaccharide (LPS; 0.9 mg/kg) was administered intravenously to induce cross-ischemic tolerance. Focal cerebral ischemia was induced 72 hours later in spontaneously hypertensive rats. Serial brain MR images were obtained 6 hours, 24 hours, 4 days, 7 days, and 14 days after ischemia by using a 7.05-tesla unit.Lesion-reducing effects were evident 6 hours after ischemia in the LPS group. Preconditioning with LPS does not merely delay but prevents ischemic cell death by reducing lesion size. Lesion reduction was a sustained effect noted up to 14 days after ischemia. Reduction of local cerebral blood flow (ICBF) in the periinfarct area was significantly inhibited in the LPS group, which was correlated with endothelial nitric oxide synthase (eNOS) expression.Conclusions. Significant preservation of ICBF in the periinfarct area, which is relevant to sustained upregulation of eNOS, could be a candidate for the long-term inhibiting effect on infarct evolution in the LPS-induced tolerant state.