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预处理皮质损伤可降低自发性高血压大鼠局灶性缺血期间梗死灶周围去极化的发生率:与先前麻醉的相互作用及高血糖的影响

Preconditioning cortical lesions reduce the incidence of peri-infarct depolarizations during focal ischemia in the Spontaneously Hypertensive Rat: interaction with prior anesthesia and the impact of hyperglycemia.

作者信息

Zhao Liang, Nowak Thaddeus S

机构信息

Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee, USA.

出版信息

J Cereb Blood Flow Metab. 2015 Jul;35(7):1181-90. doi: 10.1038/jcbfm.2015.37. Epub 2015 Mar 11.

DOI:10.1038/jcbfm.2015.37
PMID:25757750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4640273/
Abstract

The relationship between peri-infarct depolarizations (PIDs) and infarction was investigated in a model of preconditioning by cortical freeze lesions (cryogenic lesions, CL) in the Spontaneously Hypertensive Rat. Small (< 5 mm(3)) lesions produced 24 hours before permanent focal ischemia were protective, without impacting baseline cerebral blood flow (CBF) and metabolism. Prior CL reduced infarct volume, associated with improved penumbral CBF as previously showed for ischemic preconditioning. The brief initial procedure avoided sham effects on infarct volume after subsequent occlusion under brief anesthesia. However, under prolonged isoflurane anesthesia for perfusion monitoring both sham and CL rats showed reduced PID incidence relative to naive animals. This anesthesia effect could be eliminated by using α-chloralose during perfusion imaging. As an additional methodological concern, blood glucose was frequently elevated at the time of the second surgery, reflecting buprenorphine-induced pica and other undefined mechanisms. Even modest hyperglycemia (>10 mmol/L) reduced PID incidence. In normoglycemic animals CL preconditioning reduced PID number by 50%, demonstrating associated effects on PID incidence, penumbral perfusion, and infarct progression. Hyperglycemia suppressed PIDs without affecting the relationship between CBF and infarction. This suggests that the primary effect of preconditioning is to improve penumbral perfusion, which in turn impacts PID incidence and infarct size.

摘要

在自发性高血压大鼠的皮层冷冻损伤(低温损伤,CL)预处理模型中,研究了梗死周围去极化(PID)与梗死之间的关系。在永久性局灶性缺血前24小时产生的小(<5 mm³)损伤具有保护作用,且不影响基线脑血流量(CBF)和代谢。如先前对缺血预处理所显示的那样,预先进行CL可减少梗死体积,并改善半暗带CBF。短暂的初始操作避免了在短暂麻醉下随后闭塞后对梗死体积的假手术影响。然而,在长时间异氟烷麻醉下进行灌注监测时,与未处理动物相比,假手术组和CL组大鼠的PID发生率均降低。在灌注成像期间使用α-氯醛糖可消除这种麻醉效果。作为另一个方法学问题,在第二次手术时血糖经常升高,这反映了丁丙诺啡诱导的异食癖和其他不明机制。即使是轻度高血糖(>10 mmol/L)也会降低PID发生率。在血糖正常的动物中,CL预处理使PID数量减少了50%,表明其对PID发生率、半暗带灌注和梗死进展具有相关影响。高血糖抑制PID,但不影响CBF与梗死之间的关系。这表明预处理的主要作用是改善半暗带灌注,进而影响PID发生率和梗死大小。

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Hyperglycemia accelerates apparent diffusion coefficient-defined lesion growth after focal cerebral ischemia in rats with and without features of metabolic syndrome.高血糖加速伴有和不伴有代谢综合征特征的大鼠局灶性脑缺血后表观扩散系数定义的病变生长。
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