右美托咪啶后处理加重大鼠离体心肌缺血再灌注损伤

摘要

目的：评价右美托咪啶后处理对大鼠离体心肌缺血再灌注损伤后心功能及梗死面积比的影响。方法30只健康雄性SD大鼠，体重200～240 g，将其随机分成5组（ n＝6）：持续灌注组（ C组）、缺血再灌注组（ I/R组）、2．4μg/L右美托咪啶后处理组（ D组）、育亨宾组（ Y组）、育亨宾＋2．4μg/L Dex后处理组（ Y＋D组）。制备离体心脏Langendorff灌注模型，各组经主动脉灌注K-H液，除C组持续灌注140 min外，其余各组均平衡灌注20 min后停灌30 min，再灌注90 min。记录平衡末、再灌注15、30及90 min时的左心室舒张末压（ LVEDP）、左心室发展压（LVDP）、左心室压力上升（或）下降最大速率（±dp/dtmax）及心率（HR）。再灌注90 min时采用2，3，5-氯三苯四唑（ TTC）染色法染心肌片并计算心肌梗死面积百分比。结果与I/R组比较，D组心率在再灌注15 min及再灌注30 min下降（P＜0．05），再灌注末恢复（P＞0．05）；心肌梗死面积比增加（P＜0．05〕。与D组比较， Y＋D组心率在再灌注15 min及再灌注30 min上升；心肌梗死面积比减少（ P＜0．05〕。结论右美托咪啶后处理使大鼠离体心肌的心率下降，心肌梗死面积比增加，其机制与激动α2-肾上腺素受体有关。%Objective To investigate the effects of dexmedetomidine post -treatment on the cardiac function and in-farct size of isolated rat hearts with acute myocardial ischemia -reperfusion ( I/R) injury.Methods Thirty pathogen-free male SD rats weighing 200-240 g were randomly divided into five groups (n=6):a control (C) group, an ische-mia-reperfusion (I/R) group, a dexmedetomidine post -treatment (D) group, a yohimbine (Y) group, and a yohim-bine+dexmedetomidine (Y+D) group.The hearts were isolated from the rats and perfused with Krebs -Henseleit buff-er ( KHB) in a Langendorff apparatus .The C group was continuously infused for 140 min, while other groups were first given 20 min of infusion followed by arresting (30 min) before 90 min of reperfusion.Then, LVEDP, LVDP, +dp/dtmax, -dp/dtmax and HR were measured and recorded at the end of first infusion and at 15, 30, and 90 min of reperfu-sion.Infarct size was determined at 90 min of reperfusion by TTC staining .Results Compared with the I/R group, the D group presented reduced HRs at 15 and 30 min of reperfusion (110 ±9 vs 230 ±14, and 102 ±6 vs 238 ±14, P<0.05), which did not reverse at the end of reperfusion (226 ±13 vs 225 ±8, P>0.05).The infarct size percentage of the D group was increased [(54.8 ±6.2)%vs (40.2 ±2.2)%, P<0.05].Compared with the D group, the rising of HR was seen in the Y+D group at 15 and 30 min of reperfusion (237 ±13 vs 110 ±9, and 235 ±11 vs 102 ±6).The infarct size percentage of the Y +D group declined [(39.8 ±3.8)% vs (54.8 ±6.2)%, P<0.05].Conclusions Dex post-treatment can reduce the heart rate of isolated rat hearts and enlarge the infarct size , which may be associated with activated α2 -Adrenergic receptors .