CAJ | 학술논문

目的观察在心肌缺血/再灌注(I/R)损伤前(预处理)或损伤后(后处理)给予脂肪乳对心脏I/R损伤的改善作用,探讨脂肪乳在心脏保护方面的潜在价值.方法实验采用大鼠Langendorff心脏离体灌流模型.将24只雄性SD大鼠随机分组:空白对照组(ISCH组)心脏离体平衡50 min,37 ℃缺血40 min,复灌120 min;脂肪乳预处理组(I-preC组)心脏离体平衡20 min,给予含30%的脂肪乳灌注液输注15 min,洗脱15 min,随后37 ℃缺血40 min,复灌120 min;脂肪乳后处理组(I-postC 组)心脏离体平衡50 min,37 ℃缺血40 min,复灌120 min,复灌开始即给予含30%的脂肪乳灌注液输注15 min.于平衡50 min和复灌120 min期间连续监测左室内压上升和下降最大速率(±dp/dt max)、左室舒张期末压(LVEDP)、左室舒张压(LVDP)、心率(HR).平衡20 min和复灌60 min时接取冠状动脉流出液,测定肌酸激酶(CK)和乳酸脱氢酶(LDH)的活性.复灌结束后计算心肌梗死面积.结果心脏机械功能指标:与ISCH组比较,复灌期间I-postC组+dp/dt max、LVDP显著升高,-dp/dt max、LVEDP显著降低(P均＜0.05);而I-preC组各指标比较差异无统计学意义.冠状动脉生化指标:复灌60 min时I-preC组和I-postC组CK和LDH活性均较ISCH组显著降低(P均d＜0.05);I-preC组与I-postC组比较差异无统计学意义(尸均＞0.05).I-preC组和I-postC组心肌梗死面积较ISCH组显著降低[(21.6±1.8)%、(15.9±1.3)%比(46.5±3.9)%,P均<0.05)];I-preC组与I-postC组比较差异无统计学意义(P＞0v.05).结论脂肪乳预处理和后处理均能减轻心肌I/R损伤后CK和LDH的释放,缩小心肌梗死面积.脂肪乳后处理能显著增强心肌I/R损伤后心脏的机械功能.
목적 관찰재심기결혈/재관주(I/R)손상전(예처리)혹손상후(후처리)급여지방유대심장I/R손상적개선작용,탐토지방유재심장보호방면적잠재개치.방법 실험채용대서Langendorff심장리체관류모형.장24지웅성SD대서수궤분조:공백대조조(ISCH조)심장리체평형50 min,37 ℃결혈40 min,복관120 min;지방유예처리조(I-preC조)심장리체평형20 min,급여함30%적지방유관주액수주15 min,세탈15 min,수후37 ℃결혈40 min,복관120 min;지방유후처리조(I-postC 조)심장리체평형50 min,37 ℃결혈40 min,복관120 min,복관개시즉급여함30%적지방유관주액수주15 min.우평형50 min화복관120 min기간련속감측좌실내압상승화하강최대속솔(±dp/dt max)、좌실서장기말압(LVEDP)、좌실서장압(LVDP)、심솔(HR).평형20 min화복관60 min시접취관상동맥류출액,측정기산격매(CK)화유산탈경매(LDH)적활성.복관결속후계산심기경사면적.결과 심장궤계공능지표:여ISCH조비교,복관기간I-postC조+dp/dt max、LVDP현저승고,-dp/dt max、LVEDP현저강저(P균＜0.05);이I-preC조각지표비교차이무통계학의의.관상동맥생화지표:복관60 min시I-preC조화I-postC조CK화LDH활성균교ISCH조현저강저(P균d＜0.05);I-preC조여I-postC조비교차이무통계학의의(시균＞0.05).I-preC조화I-postC조심기경사면적교ISCH조현저강저[(21.6±1.8)%、(15.9±1.3)%비(46.5±3.9)%,P균<0.05)];I-preC조여I-postC조비교차이무통계학의의(P＞0v.05).결론 지방유예처리화후처리균능감경심기I/R손상후CK화LDH적석방,축소심기경사면적.지방유후처리능현저증강심기I/R손상후심장적궤계공능.
Objective To investigate whether intralipid could protect perfused hearts of rats against ischemia/reperfusion(I/R)injury when it was administered before(preconditioning)or after the adverse ischemic event(postconditioning),in order to ascertain if intralipid would be a novel therapeutic strategy for myocardial I/R injury.Methods Studies were conducted in Langendorff-perfused isolated rat hearts.Twenty-four male Sprague-Dawley(SD)rats were divided into 3 groups randomly.The experimental procedure consisted of balance perfusion for 50 minutes,warm global ischemia(37℃)for 40 minutes and 120 miuntes of reperfusion.Preconditioning of hearts in myocardial preconditioning(I-preC group)consisted of 1 5 minutes of intralipid followed bv 1 5 minutes of wash out before ischemia for 40 minutes and reperfusion for 120 minutes.In myocardial postconditioning(I-postC group)rat hearts were perfused with intralipid for 15 minutes at the onset of reperfusion.Hearts without intralipid treatment served as ischemic control (ISCH)group.Left ventricular mechanical function(heart rate(HR),left ventricular end-diastolic pressure (LVEDP),left ventricular diastolic pressure(LVDP),maximal change rate of intraventricular pressure rise/down(±dp/dt max)]were measured during the experiment.cardiac enzyme activity[creatine kinase (CK),lactate dehydrogenase(LDH)]were determined at 20 minutes after balance and 60 minutes after reperfusion.Results Comparing with ISCH group,the LVDP and+dp/dt max in the I-postC group were significantly higher and LVDEP,-dp/dt max were lower when compared with ISCH groups during reperfusion(all P＜0.05＝.There were no significant differences in above indexes in I-preC group.As compared with the ISCH group,the content of LDH and CK in I-preC and I-postC were significantly lower at 60 minutes after reperfusion(all P＜0.05＝.However.there were no significant differences between the I-preC and I-postC groups with respect to the levels of LDH and CK.The infarct size(IS)pf I-preC and I-postC was markedly smaller than that of the ISCH group at 120 minutes of reperfusion[(21.6±1.8)%,(15.9±1.3)%vs.(46.5±3.9)%,both P＜0.05＝.The IS did not differ between the I-preC and I-postC groups(P＞0.05).Conclusion Intralipid administered before or after ischemia can decrease the level of CK,LDH and IS during reperfusion in isolated rat hearts. Intralipid postconditioning improves mechanical function.