定量组织速度显像技术评价缺血后适应对急性缺血再灌注犬心脏的保护作用
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摘要
目的:
1探讨定量组织速度显像(quantitative tissue velocity imaging,QTVI)技术评价急性心肌缺血再灌注犬心功能变化的可行性、准确性,为临床提供一种可评估心脏室壁运动和心功能的简便、客观方法。
2探讨缺血后适应(ischemic-postconditioning,IPostC)方法的可行性、安全性及减轻急性心肌缺血再灌注损伤(myocardium ischemia-reperfusion injury,MIRI)的有效性,从而为临床提供一种操作简单、可减轻急性心肌梗死再灌注治疗损伤的新思路。
3探讨缺血后适应与氧自由基(oxygen free radical,OFR)的关系。
方法:
将21只杂种犬随机分为三组:对照组(Con组,n=7):结扎左前降支(left anterior descending artery, LAD )1小时,再灌注3小时;缺血预适应组(Pre-C组, n=7):结扎左前降支1小时前行缺血预适应(5分钟结扎/5分钟再灌注的4次循环);缺血后适应组(Post-C组,n=7):结扎左前降支1小时后,再灌注前行缺血后适应(30秒再灌/30秒再闭的3次循环)。实验犬分别于缺血前基础状态、缺血60分钟、再灌注60分钟、再灌注120分钟、再灌注180分钟行以下各项检查。
心脏收缩功能指标:包括收缩期心肌运动峰值速度(systolic peak velocity ,Vs)、峰值位移(systolic peak displacement,Vs)、短轴缩短率(Fraction of Shorten,FS)、左室射血分数(ejective fraction of left ventricle,EF ),通过GE Vivid7彩色超声显像系统检查。其中FS以直线解剖M型超声心动图获得,EF值采用单平面Simpson’s法测得。在组织速度成像(tissue velocity imaging,TVI)状态下,于心尖四腔心、心尖两腔心、左室长轴切面,取样容积置于二尖瓣环处,分别获取侧壁、后间隔、前壁、下壁、前间隔、后壁的Vs、Ds值,计算6个壁Vs、Ds平均值作为左室整体收缩功能。
心肌梗死范围:以血清肌酸激酶(creatine kinase,CK)和大体标本2%氯化三苯四氮唑(triphenyl tetrazolium chloride,TTC)染色评价:分别于实验前、实验结束时抽取静脉血测定CK。实验结束后处死犬,重新阻断LAD原闭塞部位,Evens blue染色区分缺血区心肌,进行TTC染色,计算AR (the area of risk)/ LV(the left ventric- ular mass),AN( the area of necrosis) /AR,反映心肌坏死程度。
氧自由基生化指标:在上述5个时间点抽静脉血检测丙二醛(malondialdehyde ,MDA)含量及超氧化物歧化酶(superoxide dismutase,SOD)活性。结果:
1.缺血60分钟后各组Vs、Ds、EF及FS值均明显下降,组间没有显著差异,再灌注180分钟后各组均有改善,Pre-C组及Post-C组明显高于Con组,P<0.05。
2.再灌注180分钟后,Pre-C组及Post-C组血清MDA含量低于Con组,P<0.05,而SOD活性高于Con组,P<0.05。
3.再灌注180分钟后各组血清CK水平均升高,Pre-C及Post-C组低于Con组,P<0.05。TTC染色显示AN/AR在Pre-C及Post-C组低于Con组,P<0.05。
结论:
1.QTVI技术可较准确评价急性心肌缺血再灌注犬心脏收缩功能变化,以其简便、客观的优点为临床提供一种可评估左室整体收缩功能的方法。
2.缺血后适应与缺血预适应相似,可以缩小犬急性心肌缺血再灌注后心肌梗死面积,促进左室整体收缩功能恢复,从而减轻心肌缺血再灌注损伤。
3.缺血后适应可能通过减少心肌缺血再灌注初期氧自由基生成达到心脏保护作用。
Objective:
To discuss the feasibility and accuracy of quantitative tissue velocity imaging (QTVI) to quantify myocardial function induced by acute ischemia and reperfusion, which will be a convenient and objective method applied for the clinic.
To discuss the feasibility,security and availability of myocardial ischemic- postconditioning(IPostC),which will be a new and practical thinking for the clinic to reduce myocardial ischemia-reperfusion injury(MIRI).
To discuss the relation between oxygen free radical(OFR) and myocardial ischemic-postconditioning.
Methods:
All animals were randomly assigned to one of three groups: control group (Con,n=7): the left anterior descending artery (LAD ) was reversibly occluded for 60 min followed by 3h of reperfusion; ischemic-preconditioning group (Pre-C, n=7):The LAD was occluded for 5 min followed by 5 min of reperfusion before the 60 min of prolonged occlusion; ischemic-postconditioning group (n=7):after 60 min of LAD occlusion, reperfusion was initiated for 30s followed by 30s of reocclusion, repeated for three cycles. Reperfusion was continued for a total of 3h in all experiments. All indexes were examinated at baseline, at the end of ischemia, and at 1, 2, 3h of reperfu- sion.
The indexes of systolic function included systolic peak velocity (Vs),systolic peak displacement(Ds),fraction of shorten(FS) and ejective fraction of left ventricle(LVEF).Vs and Ds were measured on anterior wall of left ventricle and inferior wall, anterior septal and post wall, post septal and lateral wall using QTVI technique; LVEF was measured using Simpson’s method and FS was measured with anatomical m-mode echocardiography. The infarct size was evaluated by blood-serum creatine kinase(CK) and patholog-
ic stain using triphenyltetrazolium chloride(TTC). Venous blood samples were with- drawn at baseline and 3h of reperfusion for measuring CK. After the heart was harve- sted, the LAD was religated in the original position, and Evens blue dye was injected for staining the nonischemic region blue and thereby outline the area of risk(AR).The- n the AR was separated from the nonischemic zone and incubated in a 2% solution of TTC to differentiate the area of necrosis(AN) from the nonnecrotic AR.The AR was expressed as a percentage of the left ventricular mass (AR/LV), and AN, as a percent- age of the AR (AN/AR), and they were calculated by tissue weight.
The indexes of OFR including blood-serum malondialdehyde(MDA) and super- oxide dismutase(SOD) were measured in each group at baseline, at the end of ischem- ia, and at 1, 2, and 3 h of reperfusion.
Results:
In all canines, Vs,Ds,EF and FS decreased significantly at the end of ischemia.At 3h of reperfusion, compared to the Con group,Vs,Ds,EF and FS were higher in the Post-C group and Pre-C group;Plasma CK and MDA were less,whereas SOD was more;the infarct size measured by TTC was smaller,and the Vs and Ds measured by QTVI well correlated with EF and FS.
Conclusions:
With convenient and objective feature,QTVI technique could evaluate systolic function exactly in acute myocardial ischemia-reperfusion injury(MIRI) in dogs.Similar to the ischemic-preconditioning,ischemic-postconditioning could decrease the area of necrosis and recover systolic function to reduce MIRI.This protection was possibly concerned with oxygen free radical.
1探讨定量组织速度显像(quantitative tissue velocity imaging,QTVI)技术评价急性心肌缺血再灌注犬心功能变化的可行性、准确性,为临床提供一种可评估心脏室壁运动和心功能的简便、客观方法。
2探讨缺血后适应(ischemic-postconditioning,IPostC)方法的可行性、安全性及减轻急性心肌缺血再灌注损伤(myocardium ischemia-reperfusion injury,MIRI)的有效性,从而为临床提供一种操作简单、可减轻急性心肌梗死再灌注治疗损伤的新思路。
3探讨缺血后适应与氧自由基(oxygen free radical,OFR)的关系。
方法:
将21只杂种犬随机分为三组:对照组(Con组,n=7):结扎左前降支(left anterior descending artery, LAD )1小时,再灌注3小时;缺血预适应组(Pre-C组, n=7):结扎左前降支1小时前行缺血预适应(5分钟结扎/5分钟再灌注的4次循环);缺血后适应组(Post-C组,n=7):结扎左前降支1小时后,再灌注前行缺血后适应(30秒再灌/30秒再闭的3次循环)。实验犬分别于缺血前基础状态、缺血60分钟、再灌注60分钟、再灌注120分钟、再灌注180分钟行以下各项检查。
心脏收缩功能指标:包括收缩期心肌运动峰值速度(systolic peak velocity ,Vs)、峰值位移(systolic peak displacement,Vs)、短轴缩短率(Fraction of Shorten,FS)、左室射血分数(ejective fraction of left ventricle,EF ),通过GE Vivid7彩色超声显像系统检查。其中FS以直线解剖M型超声心动图获得,EF值采用单平面Simpson’s法测得。在组织速度成像(tissue velocity imaging,TVI)状态下,于心尖四腔心、心尖两腔心、左室长轴切面,取样容积置于二尖瓣环处,分别获取侧壁、后间隔、前壁、下壁、前间隔、后壁的Vs、Ds值,计算6个壁Vs、Ds平均值作为左室整体收缩功能。
心肌梗死范围:以血清肌酸激酶(creatine kinase,CK)和大体标本2%氯化三苯四氮唑(triphenyl tetrazolium chloride,TTC)染色评价:分别于实验前、实验结束时抽取静脉血测定CK。实验结束后处死犬,重新阻断LAD原闭塞部位,Evens blue染色区分缺血区心肌,进行TTC染色,计算AR (the area of risk)/ LV(the left ventric- ular mass),AN( the area of necrosis) /AR,反映心肌坏死程度。
氧自由基生化指标:在上述5个时间点抽静脉血检测丙二醛(malondialdehyde ,MDA)含量及超氧化物歧化酶(superoxide dismutase,SOD)活性。结果:
1.缺血60分钟后各组Vs、Ds、EF及FS值均明显下降,组间没有显著差异,再灌注180分钟后各组均有改善,Pre-C组及Post-C组明显高于Con组,P<0.05。
2.再灌注180分钟后,Pre-C组及Post-C组血清MDA含量低于Con组,P<0.05,而SOD活性高于Con组,P<0.05。
3.再灌注180分钟后各组血清CK水平均升高,Pre-C及Post-C组低于Con组,P<0.05。TTC染色显示AN/AR在Pre-C及Post-C组低于Con组,P<0.05。
结论:
1.QTVI技术可较准确评价急性心肌缺血再灌注犬心脏收缩功能变化,以其简便、客观的优点为临床提供一种可评估左室整体收缩功能的方法。
2.缺血后适应与缺血预适应相似,可以缩小犬急性心肌缺血再灌注后心肌梗死面积,促进左室整体收缩功能恢复,从而减轻心肌缺血再灌注损伤。
3.缺血后适应可能通过减少心肌缺血再灌注初期氧自由基生成达到心脏保护作用。
Objective:
To discuss the feasibility and accuracy of quantitative tissue velocity imaging (QTVI) to quantify myocardial function induced by acute ischemia and reperfusion, which will be a convenient and objective method applied for the clinic.
To discuss the feasibility,security and availability of myocardial ischemic- postconditioning(IPostC),which will be a new and practical thinking for the clinic to reduce myocardial ischemia-reperfusion injury(MIRI).
To discuss the relation between oxygen free radical(OFR) and myocardial ischemic-postconditioning.
Methods:
All animals were randomly assigned to one of three groups: control group (Con,n=7): the left anterior descending artery (LAD ) was reversibly occluded for 60 min followed by 3h of reperfusion; ischemic-preconditioning group (Pre-C, n=7):The LAD was occluded for 5 min followed by 5 min of reperfusion before the 60 min of prolonged occlusion; ischemic-postconditioning group (n=7):after 60 min of LAD occlusion, reperfusion was initiated for 30s followed by 30s of reocclusion, repeated for three cycles. Reperfusion was continued for a total of 3h in all experiments. All indexes were examinated at baseline, at the end of ischemia, and at 1, 2, 3h of reperfu- sion.
The indexes of systolic function included systolic peak velocity (Vs),systolic peak displacement(Ds),fraction of shorten(FS) and ejective fraction of left ventricle(LVEF).Vs and Ds were measured on anterior wall of left ventricle and inferior wall, anterior septal and post wall, post septal and lateral wall using QTVI technique; LVEF was measured using Simpson’s method and FS was measured with anatomical m-mode echocardiography. The infarct size was evaluated by blood-serum creatine kinase(CK) and patholog-
ic stain using triphenyltetrazolium chloride(TTC). Venous blood samples were with- drawn at baseline and 3h of reperfusion for measuring CK. After the heart was harve- sted, the LAD was religated in the original position, and Evens blue dye was injected for staining the nonischemic region blue and thereby outline the area of risk(AR).The- n the AR was separated from the nonischemic zone and incubated in a 2% solution of TTC to differentiate the area of necrosis(AN) from the nonnecrotic AR.The AR was expressed as a percentage of the left ventricular mass (AR/LV), and AN, as a percent- age of the AR (AN/AR), and they were calculated by tissue weight.
The indexes of OFR including blood-serum malondialdehyde(MDA) and super- oxide dismutase(SOD) were measured in each group at baseline, at the end of ischem- ia, and at 1, 2, and 3 h of reperfusion.
Results:
In all canines, Vs,Ds,EF and FS decreased significantly at the end of ischemia.At 3h of reperfusion, compared to the Con group,Vs,Ds,EF and FS were higher in the Post-C group and Pre-C group;Plasma CK and MDA were less,whereas SOD was more;the infarct size measured by TTC was smaller,and the Vs and Ds measured by QTVI well correlated with EF and FS.
Conclusions:
With convenient and objective feature,QTVI technique could evaluate systolic function exactly in acute myocardial ischemia-reperfusion injury(MIRI) in dogs.Similar to the ischemic-preconditioning,ischemic-postconditioning could decrease the area of necrosis and recover systolic function to reduce MIRI.This protection was possibly concerned with oxygen free radical.
引文
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[50] Iliodromitis EK,Georqiadis M,Cohen MV,et al.Protection from postconditioning depends on the number of short ischemic insults in anesthetized pigs[J]. Basic Res Cardiol. 2006 Nov;101(6):502-7.
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[4] Feng JH, Fischer G, Lucchinetti E, et al. Infarct-remodeled myocardium is receptive to protection by isoflurane postconditioning: role of protein kinase B/Akt signaling.Infarct-remodeled Myocardium Is Receptive to Protection by Isoflurane Postconditioning: Role of Protein Kinase B/Akt Signaling[J]. Anesthesiology, 2006,104(5):1004-1014.
[5]Tessier-Vetzel D, Tissier R, Waintraub X,et al. Isoflurane inhaled at the onset of reperfusion potentiates the cardioprotective effect of ischemic postconditioning through a NO-dependent mechanism[J]. J Cardiovasc Pharmacol,2006,47(3):487-492.
[6] Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion : comparison with ischemic preconditioning[J]. Am J Physiol Heart Circ Physiol, 2003, 285(2):H579-588.
[7] Tsang A, Hausenloy DJ, Mocanu MM, et al. Postconditioning: a form of “modified reperfusion” protects myocardium by activating the PI3K-Akt pathway[J]. Circ Res, 2004, 95(3):230–232.
[8]Yang XM, Proctor JB, Cui L, et al.Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways[J].J Am Coll Cardiol, 2004,44(5):1103-1110.
[9] Kloner RA,Dow J,Bhandari A.Postconditioning markedly attenuates ventricular arrhythmias after ischemia-reperfusion[J].J Cardiovasc Pharmacol Ther, 2006,11(1): 55-63.
[10]Schwartz LM . lschemic postconditioning during reperfusion fails to protect againstlethal myocardial ischemla-repefusion injury in pigs[abstract].Circulation,2004,l10 (supplⅢ):106
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[12]张兴华,李春梅,马晓静,等.肢体与心肌缺血后处理急性心肌缺血再灌注损伤的对比研究.中华医学杂志, 2006,86(12):841-845.
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[1] Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium[J]. Circulation,1986,74(5):1124-1136.
[2] Pagel PS, Krolikowski JG, Neff DA, et al. Inhibition of glycogen synthase kinase enhances isoflurane-induced protection against myocardial infarction during early reperfusion in vivo[J]. Anesth Analg, 2006,102(5):1348-1354.
[3] Hauser B, Bracht H, Matejovic M, et al. Nitric oxide synthase inhibition in sepsis? Lessons learned from large-animal studies[J]. Anesth Analg, 2005,101(2):488-498.
[4] Feng JH, Fischer G, Lucchinetti E, et al. Infarct-remodeled myocardium is receptive to protection by isoflurane postconditioning: role of protein kinase B/Akt signaling.Infarct-remodeled Myocardium Is Receptive to Protection by Isoflurane Postconditioning: Role of Protein Kinase B/Akt Signaling[J]. Anesthesiology, 2006,104(5):1004-1014.
[5]Tessier-Vetzel D, Tissier R, Waintraub X,et al. Isoflurane inhaled at the onset of reperfusion potentiates the cardioprotective effect of ischemic postconditioning through a NO-dependent mechanism[J]. J Cardiovasc Pharmacol,2006,47(3):487-492.
[6] Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion : comparison with ischemic preconditioning[J]. Am J Physiol Heart Circ Physiol, 2003, 285(2):H579-588.
[7] Tsang A, Hausenloy DJ, Mocanu MM, et al. Postconditioning: a form of “modified reperfusion” protects myocardium by activating the PI3K-Akt pathway[J]. Circ Res, 2004, 95(3):230–232.
[8]Yang XM, Proctor JB, Cui L, et al.Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways[J].J Am Coll Cardiol, 2004,44(5):1103-1110.
[9] Kloner RA,Dow J,Bhandari A.Postconditioning markedly attenuates ventricular arrhythmias after ischemia-reperfusion[J].J Cardiovasc Pharmacol Ther, 2006,11(1): 55-63.
[10]Schwartz LM . lschemic postconditioning during reperfusion fails to protect againstlethal myocardial ischemla-repefusion injury in pigs[abstract].Circulation,2004,l10 (supplⅢ):106
[11] Staat P, Rioufol G, Piot C, et al. Postconditioning the human heart[J]. Circulation, 2005,112(14):2143–2148.
[12]张兴华,李春梅,马晓静,等.肢体与心肌缺血后处理急性心肌缺血再灌注损伤的对比研究.中华医学杂志, 2006,86(12):841-845.
[13] 马春燕 张立敏 任卫东等。心肌声学造影评价缺血后处理对犬顿抑心肌微血管内皮功能的保护作用[J]。中国超声医学杂志 2006年第22卷第8期:570-573.
[14] 袁志柳 刘兴德 陈保林等。缺血后处理对缺血再灌注大鼠心肌梗死面积、CK、MDA及SOD的影响 [J]。循环医学杂志 2006,16(2):27～31.
[15] Halestrap AP,Clarke SJ,Javadov SA, et al. Mitochondrial permeability transition pore opening during myocardial reperfusion-a target for cardioprotection[J]. Cardiovasc Res,2004,61(3):372–385.
[16] Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion[J]. Cardiovasc Res, 2004,62(1):74–85.
[17] Krolikowski JG, Weihrauch D, Bienengraeber M, et al. Role of Erk1/2, p70s6K, and eNOS in isoflurane-induced cardioprotection during early reperfusion in vivo[J].Can J Anaesth, 2006,53(2):174-182.
[18] Feng J, Lucchinetti E, Ahuja P, et al. Isoflurane postconditioning prevents opening of the mitochondrial permeability transition pore through inhibition of glycogen synthase kinase-3β[J]. Anesthesiology, 2005,103(5):987–995.
[19] Fischer U, Schulze-Osthoff K. New approaches and therapeutics targeting apoptosis in disease[J]. Pharmacol Rev, 2005,57(2):187–215.