Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion in rats

Abstract

BackgroundExperimental studies have shown that ischemic postconditioning can reduce neuronal injury in the setting of cerebral ischemia, but the mechanisms are not yet clearly elucidated. This study was conducted to determine whether ischemic postconditioning can alter expression of heat shock protein 70 and reduce acute phase neuronal injury in rats subjected to transient focal cerebral ischemia/reperfusion.MethodsFocal cerebral ischemia was induced by intraluminal middle cerebral artery occlusion for 60 min in twenty male Sprague-Dawley rats (250-300 g). Rats were randomized into control group and an ischemic postconditioning group (10 rats per group). The animals of control group had no intervention either before or after MCA occlusion. Ischemic postconditioning was elicited by 3 cycles of 30 s reperfusion interspersed by 10 s ischemia immediately after onset of reperfusion. The infarct ratios, brain edema ratios and motor behavior deficits were analyzed 24 hrs after ischemic insult. Caspase-3 reactive cells and cells showing heat shock protein 70 activity were counted in the caudoputamen and frontoparietal cortex.ResultsIschemic postconditiong did not reduce infarct size and brain edema ratios compared to control group. Neurologic scores were not significantly different between groups. The number of caspase-3 reactive cells in the ischemic postconditioning group was not significantly different than the value of the control group in the caudoputamen and frontoparietal cortex. The number of cells showing heat shock protein 70 activity was not significantly different than the control group, as well.ConclusionsThese results suggest that ischemic postconditioning may not influence the early brain damage induced by focal cerebral ischemia in rats.

The infarct‐limiting effect of cerebral ischaemic postconditioning in rats depends on the middle cerebral artery branching pattern

“…Previous studies demonstrated that the effectiveness of ischaemic PostCon strongly depends on the specific protocol employed. For example, Kim et al (2010) did not note any neuroprotective effect of PostCon elicited by three episodes of 10-s MCA occlusion and 30-s reperfusion after 60-min intraluminal MCA occlusion in rats. In contrast, a robust neuroprotective effect was found after application of six cycles of 30-s ischaemia/30-s reperfusion in the same model (Xing et al 2008).…”

Comparative morphometric characteristics of edema-swelling manifestations in the amygdala of adult white rats after 20-, 30-, and 40-min common carotid artery occlusion

“…Некоторые авторы склонны видеть в процессе отёка-набухания мозга проявления естественного защитного механизма и санации нервной ткани по типу лимфатического дренажа отростками астроцитов. Отёк-набухание мозга, по существу, является частично обратимой плейотропной реакцией на фоне незначительных повреждений структур и необратимой при тяжёлых изменениях нервной ткани (например, пикноморфные гомогенизированные нейроны, клетки тени) [12,16].…”

Whole-scale neurobehavioral assessments of photothrombotic ischemia in freely moving mice

“…The sections were mounted onto coverslip and photographed with a digital camera. The ischemia size were then analyzed with picture analysis software (Adobe Photoshop CS5) and expressed as a percentage of the pixels of the infarct area relative to the pixels of the whole slice (Kim et al, 2010;Zhao et al, 2003), computed according to the following formula: %Ischemia size = pixels of the infarct area pixels of the whole slice × 100%…”