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作 者:董红燕[1] 朱珊珊[2] 于红丽[1] 张中明[3]
机构地区:[1]徐州医学院神经生物学研究中心,江苏徐州221002 [2]徐州医学院麻醉医学研究所 [3]徐州医学院附属医院胸心外科,江苏徐州221002
出 处:《徐州医学院学报》2004年第2期102-105,共4页Acta Academiae Medicinae Xuzhou
基 金:江苏省重点实验室开放课题资助项目 (K984 3)
摘 要:目的 观察缺血预处理 (IP)复合 32℃浅低温及晶体停搏液保护对缺血再灌注损伤未成熟心肌细胞内Ca2 + 分布的影响。方法 应用Langendorff离体心脏灌注模型 ,IP采用 2次 5min缺血、5min再灌注 ,实验分为IP+32℃浅低温组和单纯 32℃浅低温组。心脏灌注St.ThomasⅡ停搏液 ,缺血 30min ,37℃再灌注 30min。进行血流动力学测定、焦锑酸钾沉淀Ca2 + 染色及心肌细胞体积密度 (Vvi)测定。结果 再灌注 30min ,IP组左心室发展压 (LVDP)、左心室压力最大上升及下降速率 (+dp dtmax、-dp dtmax)恢复率明显高于单纯 32℃浅低温组 (P <0 .0 5 ) ,IP组受损严重心肌细胞Vvi显著小于对照组 (P <0 .0 5 )再灌注后 ,细胞核Ca2 + 沉积随细胞损伤程度加重而增加 ,其中 32℃浅低温组细胞核Ca2 + 沉积较为明显。结论 缺血再灌注期间 ,未成熟心肌细胞内Ca2 + 分布异常与超微结构的改变有密切关系。IPObjective To study the distribution of calcium in myocardial cells in immature rabbit hearts under protection of ischemic preconditioning (IP) with mild hypothermia and crystalloid cardioplegia. Methods Langendorff model of isolated neonatal rabbit heart was subjected to IP for two times, and then arrested with St. Thomas Ⅱ cardioplegic solution. After 30 minutes of ischemia at 32 ℃ and 30 minutes of reperfusion at 37 ℃, cardiac hemodynamics, distribution of calcium and stereological quantization of myocardial cells were determined. Results The recoveries of LVDP, +dp/dt max and-dp/dt max after 30-minute reperfusion were significantly higher in IP group than in the control (P<0.05). The volume density (Vvi) of severely destroyed myocardial cells were significantly less in IP group than in control group(P<0.05). The calcium particles were mainly deposited in nuclei, and their density was proportional to the severity of celluar injury. Conclusion During ischemia reperfusion injury,the Ca 2+ distribution inside immature myocardial cells correlates with the changes of myocardial ultrastructures. IP plus 32 ℃ mild hypothermia and crystalloid cardioplegia can well protect the immature myocardium against reperfusion damage.
关 键 词:缺血预处理 浅低温晶体停搏液 IP 未成熟心肌细胞 Ca^2+分布 心肌保护
分 类 号:R331.3[医药卫生—人体生理学]
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