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Early-onset tolerance in rat global cerebral ischemia induced by a mitochondrial inhibitor.

机译:线粒体抑制剂诱导的大鼠全脑缺血的早期发作耐受性。

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摘要

It was studied whether a subtoxic dose of the mitochondrial neurotoxin, 3-nitropropionic acid (3-NPA), can initiate early-onset tolerance induction for subsequent ischemic injury. Wistar rats were pretreated for 3 h by intraperitoneal 3-NPA (20 mg/kg body weight; n=13) or solvent (n=12). Fifteen minutes global cerebral ischemia was induced by bilateral carotid artery occlusion and hypobaric hypotension. rCBF and tissue hemoglobin oxygen saturation were measured by laser Doppler scanning and a microspectrophotometric method. Ischemic insult and brain temperature were identical in both groups. Body weight and neurological scores recovered in the pretreated group but further deteriorated in the non-treated group (P<0.05). Quantitative histology demonstrated a better neuronal density in neocortex and hippocampal CA2, CA3, and CA4 of pretreated animals (P<0.05).
机译:研究了亚毒性剂量的线粒体神经毒素3-硝基丙酸(3-NPA)是否可以引发对早期缺血性损伤的早期耐受耐受。 Wistar大鼠通过腹膜内3-NPA(20 mg / kg体重; n = 13)或溶剂(n = 12)预处理3小时。双侧颈动脉闭塞和低压低血压可诱发15分钟的整体性脑缺血。通过激光多普勒扫描和显微分光光度法测量rCBF和组织血红蛋白氧饱和度。两组的缺血性损伤和脑温均相同。体重和神经学评分在预处理组中有所恢复,但在未治疗组中进一步恶化(P <0.05)。定量组织学显示,预处理动物的新皮层和海马CA2,CA3和CA4中神经元密度更好(P <0.05)。

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