71%;大肠癌微淋巴管密度(microlymphatic density,MLD)显著高于正常大肠组织(t=3.624,P<0.01)。结论大肠癌β-catenin异位表达可能是诱导大肠癌淋巴管生成的重要原因。
目的探讨舒芬太尼后处理对在体大鼠心肌缺血再灌注损伤的影响。方法健康雄性SD大鼠经结扎冠状动脉左前降支制备心肌缺血再灌注损伤模型后随机分为8组:假手术(A)组:只穿线,不结扎;缺血再灌注(B)组:缺血30min,再灌注120

min,再灌注前5 min单次静脉注射生理盐水1 ml;缺血后处理(C)组:缺血30 min末行缺血10 s,再灌注10 s,重复3次后再灌注120 min;舒芬太尼后处理(D～H)组:再灌注前5 min分别单次静脉注射舒芬太尼0.1、0.3、1、3、10μg/kg,5 min后再灌注120 min。于结扎线缝好后平衡30 min(T0)、缺血30 min末(T1)、后处理末(T2)、再灌注120min末(T3)记录血流动力学参数。计算心肌梗死面积(IS)与缺血危险区(AAR)比值(IS/AAR)。选取A、B、C、最佳剂量舒芬太尼后处理组于T3时取颈动脉血2 ml,采用硫代巴比妥酸(TBA)法测定丙二醛(MDA)浓度,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性。结果与B组比较,C、E、F、G、H组IS/AAR降低(P<0.05);与B组比较,C、F组MDA降低,SOD活性升高(P<0.05)。结论舒芬太尼可模拟缺血后处理减轻在体大鼠心肌缺血再灌注损伤,并且呈剂量依赖性。
Reperfusion A-1210477分子量 therapy must be applied as soon as possible to attenuate the ischemic insult of acute myocardial infarction(AMI).However reperfusion is responsible for 所以 additional myocardial damage,which likely involves opening of the mitochondrial permeability transition pore(mPTP).In reperfusion injury,mitochondrial

damage is a determining factor in causing loss of cardiomyocyte function and viability.Major mechanisms of mitochondrial dysfunction include the long lasting opening of mPTPs and the oxidative stress resulting from formation of reactive oxygen species(ROS).Several signaling 不 cardioprotective pathways are activated by stimuli such as preconditioning and postconditioning,obtained with brief intermittent ischemia or with pharmacological agents.These pathways converge on a common target,the mitochondria,to preserve their function after ischemia/reperfusion.The

present review discusses the role of mitochondria in cardioprotection,especially the involvement of adenosine triphosphate-dependent potassium channels,ROS signaling,and the mPTP.Ischemic postconditioning has emerged as a new way to target the mitochondria,and to drastically reduce lethal reperfusion injury.Several clinical studies using ischemic postconditioning during angioplasty now support its protective effects,and an interesting alternative is pharmacological postconditioning.In fact ischemic postconditioning and the mPTP desensitizer,cyclosporine A,have been shown to induce comparable protection in AMI patients.