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作 者:赖峻松[1] 张良成[1] 王惠枢[1] 林鹏焘[1] 陈文华[1]
机构地区:[1]福建医科大学附属协和医院麻醉科,福建福州350001
出 处:《南方医科大学学报》2014年第11期1680-1683,共4页Journal of Southern Medical University
基 金:福建省基金高校专项(C0440007)
摘 要:目的观察不同吸入浓度七氟醚预处理对脓毒症大鼠心肌细胞凋亡及炎性反应的影响,初步探讨其心肌保护作用的可能机制。方法健康成年雄性SD大鼠40只,随机分为4组(n=10):对照组(C组)、LPS组(L组)、低浓度七氟醚预处理组(S1组)、高浓度七氟醚预处理组(S2组)。采用腹腔注射LPS方法制造大鼠脓毒症模型,并于LPS注射后12 h收集大鼠心肌及血液标本,光镜下观察心肌组织常规病理形态学改变,末端标记(TUNEL)法检测细胞凋亡,ELISA法检测大鼠血清肌钙蛋白(cTnI)含量及心肌组织肿瘤坏死因子(TNF-α)含量。结果与C组比较,L组、S1组、S2组大鼠血清cTnI水平、心肌细胞凋亡指数及TNF-α含量增加(P<0.05);与L组比较,S1组、S2组大鼠血清cTnI水平、心肌细胞凋亡指数及TNF-α含量减少(P<0.05);与S1组比较,S2组大鼠各项指标水平更进一步降低(P<0.05)。结论七氟醚预处理可浓度依赖性地减轻LPS引起的心肌损伤,其机制可能与减少心肌细胞凋亡及减轻心肌局部炎症有关。Objective To observe the effects of preconditioning with different concentrations of sevoflurane on cariomyocyte apoptosis and myocardial inflammation in rats with sepsis and explore the possible mechanism of sevoflurane for myocardial protection. Methods Forty adult male Sprague-Dawley rats were randomly divided into 4 groups(n=10), namely the control group, LPS group, low- concentration sevoflurane group and high- concentration sevoflurane group. Following sevoflurane pretreatment for 30 min and a washout period for 10 min, all the rats received intraperitoneal injection of LPS or normal saline(NS) and were sacrificed 12 h later to observe the myocardial histopathology. Apoptosis of the ardiomyocytes was detected with TUNEL assay, and enzyme- linked immunosorbent assay was used to detect serum cTnI level and myocardial TNF- αlevel. Results Compared with the control group, the rats in the other 3 groups showed significantly increased serum cTnI level, myocardial TNF- α content, and apoptotic index of the cardiomyocytes(P〈0.05). Compared with those in LPS group,serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes were significantly decreased in the two sevoflurane preconditioning groups(P〈0.05), and the effect was more obvious with a high dose of sevoflurane(P〈0.05).Conclusion Sevoflurane preconditioning can concentration- dependently reduce LPS- induced myocardial injury in rats possibly by decreasing cardiomyocyte apoptosis and alleviating myocardial inflammations.
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