CAJ | 학술논문

目的：探讨乌司他丁对心搏骤停-心肺复苏大鼠心脏的保护效应及改善心功能不全的机制。方法随机将20只SD大鼠分为3组：假手术组（不进行窒息及心肺复苏，仅进行麻醉和气管切开插管、血管穿刺；A组n＝8）；对照组（静脉注射生理盐水4mL·kg-1；B组n＝6）；考察组（乌司他丁5万U·kg-1＋生理盐水3mL·kg-1，5万U配制成1mL；C组n＝6）；采用实验设计模型考察大鼠复苏前后实验设定时间段白细胞介素-12（IL-12）、心肌肌钙蛋白T（cTNT）、肿瘤坏死因子-α（TNF-α）、脑钠肽（BNP）、平均动脉压（MAP）、左室内压最大上升和下降速率（±LVdp．dt-1max）及左室舒张末压（LVEDP）的变化。结果与A组及复苏前比较，B、C组复苏后6hIL-12、cTNT、TNF-α、BNP、LVEDP等均有不同程度升高（P＜0．01），而±LVdp．dt-1max值降低（P＜0．01）；与B组比较，C组复苏后6hIL-12、cTNT、TNF-α、BNP、LVED值低于B组，而±LVdp．dt-1max值高于B组（P＜0．01）；B组复苏后6hMAP值低于复苏前、同时间A组和C组（P＜0．01）。结论乌司他丁可抑制炎症介质释放，减轻心搏骤停-心肺复苏实验大鼠心肌损伤，从而改善心搏骤停-心肺复苏实验大鼠心脏功能不全。
목적：탐토오사타정대심박취정-심폐복소대서심장적보호효응급개선심공능불전적궤제。방법수궤장20지SD대서분위3조：가수술조（불진행질식급심폐복소，부진행마취화기관절개삽관、혈관천자；A조n＝8）；대조조（정맥주사생리염수4mL·kg-1；B조n＝6）；고찰조（오사타정5만U·kg-1＋생리염수3mL·kg-1，5만U배제성1mL；C조n＝6）；채용실험설계모형고찰대서복소전후실험설정시간단백세포개소-12（IL-12）、심기기개단백T（cTNT）、종류배사인자-α（TNF-α）、뇌납태（BNP）、평균동맥압（MAP）、좌실내압최대상승화하강속솔（±LVdp．dt-1max）급좌실서장말압（LVEDP）적변화。결과여A조급복소전비교，B、C조복소후6hIL-12、cTNT、TNF-α、BNP、LVEDP등균유불동정도승고（P＜0．01），이±LVdp．dt-1max치강저（P＜0．01）；여B조비교，C조복소후6hIL-12、cTNT、TNF-α、BNP、LVED치저우B조，이±LVdp．dt-1max치고우B조（P＜0．01）；B조복소후6hMAP치저우복소전、동시간A조화C조（P＜0．01）。결론오사타정가억제염증개질석방，감경심박취정-심폐복소실험대서심기손상，종이개선심박취정-심폐복소실험대서심장공능불전。
Objective To investigate the protective effects of ulinastatin on the hearts of rats with anoxia-induced cardiac arrest-cardiopulmonary resuscitation(CA-CPR) and the mechanism of improving cardiac dysfunction .Methods Twenty male Sprague Dawley(SD) rats were randomly divided into three experimental groups :sham operation group (group A ,n= 8 ,only anesthesia , tracheotomy tube and vascular puncture) ,control group(group B ,n= 6 ,normal saline 4 mL · kg -1 injected via vein) ,Ulinastatin treatment group(group C ,n=6 ulinastatin 50 000 U/kg+normal saline 3 mL · kg -1 injected via vein);Factors including mean arte-rial pressure(MAP) ,left ventricular end diastolic pressure(LVEDP) ,the maximum rising and falling rates of left ventricular deep pressure(± LVdp .dt-1max) ,brain natriuretic peptide(BNP) ,cardiac troponin T(cTNT) ,IL-12 and TNF-αwere observed at setting time before and after cardiopulmonary resuscitation in rats .Results Compared with those of the group A and before CA-CPR ,the concentrations of IL-12、cTNT、TNF-α、BNP、and LVEDP increased(P<0 .01)while ± LVdp .dt-1max decreased(P<0 .01) at 6 h after CA-CPR in group B ,C .Compared with those of group B ,the concentrations of IL-12、CTNT、TNF-α、BNP and LVEDP of 6 h after CA-CPR in group C were lower and ± LVdp .dt-1max was higher(P<0 .01) ,The concentrations of MAP of 6 h after CA-CPR in group B was lower Compared with that of group A ,C and before CA-CPR(P<0 .01) .Conclusion Ulinastatin can improve cardiac dysfunction by depressing mediators of inflammation and reducing myocardial injury .