CAJ | 학술논문

目的：评价缺血时间因素对舒芬太尼后处理减轻大鼠心肌缺血再灌注损伤效应的影响。方法雄性SD大鼠，体重230～250 g ，采用Langendorff灌注装置制备离体心脏灌注模型。取离体心脏48个，平衡灌注30 min ，采用随机数字表法，将其分为6组（ n＝8）：I/R1-3组分别心肌缺血30、45和60 min ，再灌注90 min；SP1-3组分别心肌缺血30、45和60 min ，再灌注90 min ，并于再灌注15 min时K-H液中加入100 nmol/L舒芬太尼行后处理。分别于平衡灌注末、再灌注15、30、60和90 min时，记录左室舒张末压（LVEDP）、左室发展压（LVDP）、左室内压最大上升和最大下降速率（± dp/dtmax ）、HR和冠脉流量（CF ）。再灌注5 min时，收集冠脉流出液，测定肌酸激酶（CK ）及乳酸脱氢酶（LDH ）的活性。再灌注90 min时，每组取5个心脏，测定心肌梗死体积。结果与平衡灌注末比较，I/R1-3组再灌注各时点LVEDP升高，LVDP、± dp/dtmax和CF均降低（ P＜0.05）；与I/R1组和I/R2组比较，I/R3组再灌注30、60和90 min时LVEDP升高，LVDP及± dp/dtmax降低，再灌注15和30 min时HR和CF降低，冠脉流出液CK、LDH的活性、心肌梗死体积升高，SP1组和SP2组再灌注30、60和90 min时LVEDP降低，LVDP、± dp/dtmax和CF升高，冠脉流出液CK和LDH的活性、心肌梗死体积降低（ P＜0.05）；与I/R3组比较，SP3组再灌注30、60和90 min时LVDP降低（ P＜0.05），冠脉流出液CK和LDH的活性、心肌梗死体积差异无统计学意义（ P＞0.05）。结论缺血30和45 min时舒芬太尼后处理可减轻大鼠心肌缺血再灌注损伤，而缺血60 min时舒芬太尼后处理无心肌保护作用。
목적：평개결혈시간인소대서분태니후처리감경대서심기결혈재관주손상효응적영향。방법웅성SD대서，체중230～250 g ，채용Langendorff관주장치제비리체심장관주모형。취리체심장48개，평형관주30 min ，채용수궤수자표법，장기분위6조（ n＝8）：I/R1-3조분별심기결혈30、45화60 min ，재관주90 min；SP1-3조분별심기결혈30、45화60 min ，재관주90 min ，병우재관주15 min시K-H액중가입100 nmol/L서분태니행후처리。분별우평형관주말、재관주15、30、60화90 min시，기록좌실서장말압（LVEDP）、좌실발전압（LVDP）、좌실내압최대상승화최대하강속솔（± dp/dtmax ）、HR화관맥류량（CF ）。재관주5 min시，수집관맥류출액，측정기산격매（CK ）급유산탈경매（LDH ）적활성。재관주90 min시，매조취5개심장，측정심기경사체적。결과여평형관주말비교，I/R1-3조재관주각시점LVEDP승고，LVDP、± dp/dtmax화CF균강저（ P＜0.05）；여I/R1조화I/R2조비교，I/R3조재관주30、60화90 min시LVEDP승고，LVDP급± dp/dtmax강저，재관주15화30 min시HR화CF강저，관맥류출액CK、LDH적활성、심기경사체적승고，SP1조화SP2조재관주30、60화90 min시LVEDP강저，LVDP、± dp/dtmax화CF승고，관맥류출액CK화LDH적활성、심기경사체적강저（ P＜0.05）；여I/R3조비교，SP3조재관주30、60화90 min시LVDP강저（ P＜0.05），관맥류출액CK화LDH적활성、심기경사체적차이무통계학의의（ P＞0.05）。결론결혈30화45 min시서분태니후처리가감경대서심기결혈재관주손상，이결혈60 min시서분태니후처리무심기보호작용。
Objective To evaluate the effects of ischemic time factors on reduction of myocardial ischemia-reperfusion injury by sulfentanil postconditioning in rats .Methods Healthy adult male Sprague-Dawley rats ,weighing 230-250 g ,were heparinized and anesthetized with intraperitoneal 5% chloral hydrate 8 ml/kg .The hearts were excised and perfused in a Langendorff apparatus with K-H solution .After 30 min of stabilization ,48 isolated rat hearts were randomly assigned into 6 groups (n=8 each) using a random number table .In I/R1-3 groups ,the hearts were subjected to 30 ,45 ,and 60 min of myocardial ischemia ,respectively ,followed by 90 min of reperfusion . In SP1-3 groups , the hearts were subjected to 30 , 45 , and 60 min of myocardial ischemia , respectively ,followed by 90 min of reperfusion ,and sulfentanil 100 nmol/L was added to K-H solution at 15 min of reperfusion for postconditioning . Left ventricular end-diastolic pressure (LVEDP ) , left ventricular developed pressure (LVDP) ,+dp/dtmax ,-dp/dtmax ,HR and coronary flow (CF) were measured at the end of equilibration and 15 ,30 ,60 and 90 min of reperfusion .Creatine kinase (CK) and lactate dehydrogenase (LDH) activities in coronary effluent were measured at 5 min of reperfusion .Myocardial infarct size was determined in 5 hearts chosen randomly at 90 min of reperfusion .Results LVEDP was significantly higher ,and LVDP , ± dp/dtmax and CF were lower at each time point of reperfusion than at the end of equilibration in I/R1-3 groups ( P<0.05) .Compared with I/R1 and I/R2 groups ,LVEDP was significantly increased ,and LVDP and ± dp/dtmax were decreased at 30 ,60 and 90 min of reperfusion ,HR and CF were decreased ,and CK and LDH activities in coronary effluent and infarct size were increased at 15 and 30 min of reperfusion in group I/R3 ,and LVEDP was significantly decreased ,LVDP , ± dp/dtmax and CF were increased ,CK and LDH activities in coronary effluent and infarct size were decreased at 30 , 60 and 90 min of reperfusion in groups SP1 and SP2 ( P< 0.05 ) . Compared with group I/R3 , LVDP was significantly decreased at 30 ,60 and 90 min of reperfusion ( P<0.05) ,and no significant change was found in CK and LDH activities in coronary effluent and infarct size in group SP3 ( P>0.05 ) .Conclusion Sulfentanil postconditioning can attenuate myocardial ischemia-reperfusion injury when the rats are subjected to 30 or 45 min of ischemia ,however ,it provides no myocardial protection when the rats are subjected to 60 min of ischemia .