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机构地区:[1]中国医科大学附属盛京医院麻醉科,沈阳110004 [2]沈阳市新兴齿科,沈阳110001
出 处:《实用药物与临床》2009年第3期156-158,共3页Practical Pharmacy and Clinical Remedies
基 金:辽宁省教育厅课题资助项目(2008792)
摘 要:目的通过建立在体大鼠肺缺血再灌注损伤模型,观察七氟烷对缺血再灌注后肺组织氧自由基(OFRs)表达的影响,探讨缺血再灌注后肺损伤和七氟烷肺保护的可能机制。方法选择96只雄性wistar大鼠,参照改良的Eppinger方法建立在体大鼠肺缺血再灌注损伤模型。共分4组,每组24只大鼠。C组:开胸游离左肺门,未行肺门阻断;IR组:阻断肺门45min后开放再灌注;Sev-C组:吸入1MAC七氟烷30min,游离肺门不阻断;Sev-IR组:吸入七氟烷30min后阻断左肺门45min,然后开放再灌注。每组包括3个时点:缺血阻断45min、再灌注60min、再灌注120min,每时点6只大鼠,另外再灌注120min时,各组另取6只大鼠行支气管灌洗。记录各时点MAP、SpO2,测定W/D、肺通透指数(LPI),生化法检测肺组织MDA、SOD和MPO含量。结果与C组和Sev-C组比较,IR组和Sev-IR组再灌注后W/D、LPI均上升(P<0.05),Sev-IR组W/D、LPI升高的程度低于IR组(P<0.05);IR组再灌注60min、120min肺组织MDA、MPO含量增加(P<0.05),SOD含量减少(P<0.05)。Sev-IR组MDA、MPO增加、SOD减少的程度都低于IR组(P<0.05)。结论肺缺血再灌注后血管通透性增加,再灌注后肺损伤的机制与OFRs产生过多有关,七氟烷预处理能抑制OFRs的生成,对再灌注后肺组织具有一定的保护作用。Objective To investigate the effect of sevoflurane on pulmonary OFRs (oxygen free radicals) in ischemia-reperfusion rats. Methods The I/R(ischemia/reperfusion) injury model of rat lung was established by Sim-ulating Eppinger method. Ninety-six adult male wistar rats weighing 250 - 350 g were randomly divided into 4 groups. group C( n = 24) : continuous perfusion without ischemia;group IR( n = 24 ) :occlusion of the left pulmonary hilum for 45 rain, followed by reperfusion; group Sev-C( n = 24) : 1 MAC sevoflurane inhalation for 30 rain before ischemia, fol- lowed by continuous perfusion; group Sev-IR( n = 24 ) : 1 MAC sevoflurane inhalation for 30 rain before ischemia, fol- lowed by ischemia-reperfusion. In every group,the indexes were measured at 45 min after lung ischemia and at 60 min, 120 min of reperfusion. Moreover,another six rats were performed for bronchial lavage at 120min of reperfusion. The lung wet-to-dry weight ratio(W/D) and lung permeability index(LPI) were calculated at time points. The values of MDA, SOD and MPO were detected by biochemical methods. Results Compared with C group and Sev-C group, W/ D and LPI increased progressively after reperfusion in rat lungs in IR group and Sev-IR group (P 〈 0.05). Moreover, compared with IR group, preadministration of sevoflurane could inhibit the increase of W/D and LPI after reperfusion ( P 〈 0. 05 ). The content of MDA and MPO in IR group increased obviously after reperfusion ( P 〈 0. 05 ), while the content of SOD decreased accordingly (P 〈 0. 05 ). The inhalation of sevoflttrane could inhibit the change of MDA, SOD and MPO after reperfusion in rat lungs ( P 〈 0. 05 ). Conclusion The pulmonary permeability increases after ischemia-reperfusion injury in rat lungs. The overdose of OFRs may be associated with the lung injury after reperfusion Pretreatment of sevoflurane can inhibit the production of OFRs, then protect the pulmonary function.
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