两种离体心脏灌注模型全心缺血前后左室功能的比较

本实验旨在观察Ｌａｎｇｅｎｄｏｒｆｆ和工作心脏两种模型下离体大鼠心肌缺血 再灌注损伤前后左心室功能的变化及其差异 ,为模型的选择提供依据。一、材料与方法1 .动物与分组 :雄性健康ＳＤ大鼠2 4只 (第二军医大学实验动物中心提供 ) ,体重 31 0～ 450 ｇ。随机分成 2组 ,每组 1 2只大鼠 ,Ⅰ组为Ｌａｎｇｅｎｄｏｒｆｆ灌流组 ,Ⅱ组为工作心脏灌流组。2 .模型建立 :大鼠戊巴比妥钠 50ｍｇ/ｋｇ体重腹腔注射麻醉后 ,迅速取出心脏 ,置于 4℃冰Ｋｒｅｂｓ Ｈｅｎｓｅｌｅｉｔ(ＫＨＢ)缓冲液内排尽心腔内血液 ,然后接上主动脉插管 ,用ＫＨＢ…     

甘利欣对大白鼠离体心脏缺血再灌注损伤的保护作用

本实验采用大白鼠离体心脏,在改良的Ｌａｎｇｅｎｄｏｒｆｆ模型上,研究甘利欣对心脏缺血再灌注损伤的保护作用及其作用机制。材料和方法选用１８０～２２０ｇ健康雄性ＳＤ大白鼠２１只,随机分３组,每组７只。对照组（Ｃ组）：用Ｋ－Ｈ液持续灌注７５分钟。缺血再灌注组（Ｉ－Ｒ组）：用Ｋ－Ｈ液灌注１５分钟后,在靠近主动脉处夹住灌注管,使全心常温（３７℃）停灌３０分钟,注意保温,再恢复灌注３０分钟。甘利欣组Ｇ组）：在处死大鼠前２小时,腹腔注射甘利欣１０ｍｇ,Ｋ－Ｈ液中含甘利欣０．２ｍｍｏｌ／Ｌ,其它同Ｉ－Ｒ组。记录…     

异丙酚对离体大鼠心脏再灌注损伤后冠脉儿茶酚胺浓度的影响

目的 通过建立离体大鼠工作心脏灌注模型,测定冠脉流出液儿茶酚胺浓度,研究异丙酚对离体大鼠心脏缺血/再灌注损伤后左室功能及心肌代谢的保护机制。方法 雄性SD大鼠40只,随机分为4组(每组10只),对照组、异丙酚10μmol/L组、50μmol/L组、100μmol/L组。建立工作心脏模型后,所有心脏全心缺血25 min,再灌注30 min。在缺血前5 min、0 min,再灌注后5、10、15、20、25和30 min分别观察心率(HR)、左室发展压与心率乘积(LVDP×HR)、冠脉流量(CF)、心排出量(CO)等心功能指标,并留取冠脉流出液测量肌酸激酶(CK)、儿茶酚胺含量。结果 缺血前,异丙酚组CO、HR、LVPSP及LVDP×HR均显著低于对照组(P<0.05);4组CK值无显著变化(P>0.05),儿茶酚胺测不出。再灌注时,异丙酚组CF、CO、HR、LVEDP、LVPSP及LVDP×HR在相应时点均比对照组恢复明显(P<0.05);异丙酚组CK值显著低于对照组(P<0.05);再灌注后,异丙酚组肾上腺素和去甲肾上腺素显著低于对照组(P<0.05);各组多巴胺含量差别不显著(P>0.05)。结论 异丙酚对离体大鼠心肌缺血/再灌注损伤具有保护作用,其机制之一可能是由于异丙酚抑制心肌缺血再灌注损伤后儿茶酚胺的释放。     

一种新的动物离体肺灌注模型的建立

肺缺血再灌注损伤（LIRI）是体外循环（CPB）后发生肺部并发症的主要原因之一。持续性的非搏动血流灌注对肺也有一定程度的损伤。本研究旨在探讨通过滚压式血泵建立一种操作较为简单并且更为接近临床实际的乳猪离体肺持续灌注和缺血再灌注模型，并比较持续性灌注与缺血再灌注对肺的保护作用。     

咪唑安定预处理对缺血-再灌注离体心脏的保护作用

目的探讨咪唑安定预处理对缺血-再灌注离体心脏的保护作用。方法采用Wistar大鼠离体心脏langendofff灌注模型。实验动物随机分为四组,每组8只：正常对照组（C组）,缺血-再灌注组（I-R组）,缺血预处理组（IPC组）,咪唑安定预处理组（MPC组）。观察咪唑安定预处理对心肌缺血-再灌注后不同时间点冠脉流出液中肌酸激酶（CK）、乳酸脱氢酶（LDH）,心肌组织中超氧化物歧化酶（SOD）、髓过氧化物酶（MPO）、丙二醛（MDA）以及再灌注性心律失常、心功能的变化。结果咪唑安定预处理可以减少心肌缺血-再灌注损伤的心肌冠脉流出液中CK、LDH的含量,提高SOD活性,降低MPO、MDA水平,并且抑制再灌注心律失常的发生,保护心功能。结论咪唑安定预处理对缺血-再灌注离体心脏具有一定的保护作用。     

异丙酚、芬太尼对离体心肌缺血再灌注损伤的影响

目的 评价异丙酚、芬太尼对离体心肌缺血再灌注损伤的作用。方法 采用离体鼠Langendroff脏模型,SD大鼠 32只,取心脏用 K-H液恒温恒压主动脉逆灌、平衡 15min,随机分为 4组:（A）脂肪乳剂对照组;（B）5μg·ml-1异丙酚组;（C）10ng·ml-1芬太尼组;（D）5μg·ml-1异丙酚加10ng·ml-1芬太尼组。用含相应药液的 K-H液灌注 10min,常温全心停灌30min,然后用含相应药液的K-H液恢复灌注30min,记录各组用药前、停灌前1min、再灌30min时心脏机械功能变化、冠脉流量以及测定再灌注30min冠脉流出液里乳酸脱氢酶（LDH）活性。结果 再灌30min时B、C、D组心功能的恢复明显好于A组,D组明显好于B、C组。LDH活性B、C、D组明显低于A组,D组明显低于B、C组。结论5μg·ml-1异丙酚、10ng·ml-1芬太尼能抑制离体心肌缺血再灌注损伤,两者复合应用其作用更强。     

离体心脏灌注模型在心肌保护研究中的应用

离体心脏灌注模型在心肌保护研究中的应用秦斌黄杰综述姚震解士胜审校自从Ｌａｎｇｅｎｄｏｒｆ［１］首次报道用哺育动物离体心脏进行心脏机械功能研究以来，在此模型基础上的各种改良的Ｌａｎｇｅｎｄｏｒｆ模型相继出现在各种动物实验中，特别是离体工作心模型的研究成...     

不同浓度人参皂甙对大鼠离体心脏缺血再灌注损伤的保护作用

人参皂甙具有细胞膜稳定性和抗炎作用,能改善急性心肌缺血所致的心脏舒张功能低于。而人参皂甙的对心肌缺血再灌注损伤的影响仍不明确,本研究拟观察不同浓度人参皂甙预处理和后处理对大鼠离体心脏缺血再灌注损伤的保护作用及其机制,为临床应用提供参考。     

1,6-二磷酸果糖对幼兔离体心脏缺血/再灌注损伤的影响

目前 ,婴幼儿心脏手术中的心肌保护主要采用成熟心肌保护的方法 ,然而 ,未成熟心肌在结构、功能和代谢方面与成熟心肌有很大差异 ,用同一种方法保护两种心肌效果必然有别 ,尤其是晶体停搏液对成熟心肌的保护效果已得到肯定 ,对未成熟心肌的保护有争议。 1,6 二磷酸果糖 (ＦＤＰ)是糖代谢的中间产物 ,对心肌的保护作用已有研究 ,加入到停搏液中能否提高未成熟心肌保护作用尚未见报道。材料和方法4周龄大白兔 2 0只 ,随机分成 2组 ,建成离体心脏左心顺灌做功模型 ,灌注液采用Ｋｒｅｄ Ｈｅｎｓｅｌｅｉｔ(Ｋ Ｈ)配方 ,左心做功 30ｍｉｎ后测…     

一种大鼠胰腺缺血再灌注模型的建立

目的 建立一种简便实用的大鼠经腹主动脉胰腺缺血再灌注模型.方法 将60只Wistar大鼠随机分为:新模型组、对照组和假手术组,每组20只.采用显微外科技术游离胰腺,胰腺灌注后阻断血流2 h,恢复再灌注后0、2、4、6 h,切取胰腺体尾部组织,检测湿/干重比、行组织病理学分析及血清淀粉酶和脂肪酶检测.结果 再灌注后,新模型组血清淀粉酶2 h(3127.80±150.85)U/L、4 h(3122.80±131.52)U/L、6 h(2585.20±161.06)U/L;血清脂肪酶2 h(446.00±181.54)U/L、4 h(517.40±165.22)U/L、6 h(475.20±170.37)U/L;均随再灌注时间延长有明显升高趋势(P＜0.05),胰腺组织病理切片呈现逐渐加重的炎细胞浸润及组织水肿(P＜0.05)等改变.结论 本模型手术操作简便、又能够较好地模拟临床胰腺缺血再灌注的过程,是研究胰腺缺血再灌注损伤的较理想动物模型.

Abstract：

Objective To build a convenient model of pancreas ischemia reperfusion injury (IRI)in rats for investigating its negative impact on pancreas. Methods Wistar rats were randomized into 4groups:(1)sham-operated animals with dissociation of the pancreatic tail-segment ( sham, n=20 ); ( 2 )control animals with dissociation of the pancrea-tic tail-segment, 30 seconds of ischemia by bcloking the abdominal aorta and flushing(control, n=20);(3) Group New model animals experienced with dissociation of the pancreatic tail-segment, flushing, 120 mins of ischemia and reperfusion (IR, n=20). The level of serum amylase and lipase, wet to weight ratio of pancreas and pathological changes of pancreas were observed at0, 2, 4, 6 hours after reperfusion. Results The level of serum amylase[2 h (3127.80±150.85) U/L, 4 h (3122.80±131.52) U/L, 6 h (2585.20±161.06) U/L]and lipase[2 h (446.00±181.54) U/L, 4 h (517.40±165.22) U/L, 6 h (475.20 ± 170.37) U/L]in Group New model were increased significantly after perfusion accordingly, The tissue damage of pancreas become more serious after perfusion. Conclusion The model shows a typical IRl on pancreas of rats. It's a ideal and clinically relevant animal model for the study of pancreas IRI after transplantation.     

大鼠肝脏离体再灌注模型的建立及改进

目的 探讨建立大鼠肝脏离体再灌注模型的方法 .方法 SD大鼠肝脏经门静脉和胆道分别插管后切取备用,以加入牛血清白蛋白和牛磺胆酸盐的克-亨(Krebs-Henseleit)液为离体再灌注液.长征-1(CZ-1)型离体再灌注系统的原型包括循环灌注系统和热交换系统2套子系统,改装后省略了热交换系统,循环灌注系统包括1个恒温水浴锅、1个数显恒流泵、1个四口烧瓶、1个液体流量计、1个自制水柱式压力计、1个由玻璃漏斗及玻璃培养皿组成的器官盛放皿、1套铁架台和包括过滤及除泡装置的1套循环管路.用改装后的CZ-1型离体再灌注系统对6只大鼠的肝脏进行120 min的再灌注,灌注过程中检测肝脏胆汁的分泌量,灌注完成后取肝组织于光镜和电镜下进行观察.结果 离体再灌注肝脏的胆汁分泌量为(0.248±0.094)μl·min-1·g-1,再灌注后肝脏组织学和肝细胞的超微结构无明显改变.结论 CZ-1型大鼠肝脏离体再灌注系统价格低廉、结构简单、性能可靠.     

Coronary blood flow and myocardial metabolism during reperfusion after hypothermic cardioplegia in the dog

There have been many studies of reperfusion injury after normothermic ischemia. However, there have been few clinically relevant studies on the nature and time course of recovery of the myocardium during reperfusion after hypothermic cardioplegia. We studied reperfusion in the isolated dog heart supported by another dog. After 2 h of cardioplegic arrest at 20 degrees C, 11 normal hearts were reperfused for 30 min at optimal coronary pressures (60-100 mm Hg mean). The following events occurred: rapid rewarming, a transient hyperemia followed by a rapid return of both coronary blood flow and myocardial oxygen consumption to normal, washout of lactate, recovery of contractility and a slight decline in ATP. Most of these events occurred during the first 15 min of reperfusion. We concluded that, in normal hearts which are well protected during hypothermic cardioplegia, reperfusion at optimal coronary pressure results in recovery of the myocardium within 15 min, with the exception of recovery of ATP levels.     

大鼠肾冷缺血再灌注损伤模型的建立

目的 建立大鼠肾冷缺血再灌注损伤(IRI)的模型.方法 封闭群SD大鼠24只,随机分为2组(n=12):A组(对照组),B组(实验组).A组切除右肾并游离左肾蒂,60 min后关闭腹腔切口.B组采用冷缺血再灌注模型,主要步骤:(1)冷灌注:右肾动脉插管对左肾原位灌注.通过右肾静脉插管将灌注液引流出体外,完成冷灌注后切除右肾,阻断左肾蒂.(2)冷缺血保存:将已充分游离的左肾牵至腹腔外,在自制保存袋中冷保存.(3)再灌注:60min后,去除保存袋,开放血流,再灌注左肾,左肾复位,缝合切口;2组大鼠均在术后24 h再次手术切除左.肾.肾组织进行光镜、电镜形态学检查,检测肾组织匀浆中超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量,术前与术后24 h取血标本进行测定血尿素氮(BUN)、肌酐(Cr)评估肾功能.结果 (1)形态学检查(光镜与电镜超微结构):A组肾脏组织形态结构正常,B组损伤表现明显;(2)A组手术前后比较血浆BUN、Cr测定值差异均无统计学意义(P＞0.05).IR后的B组均高于术前,差异有统计学意义(P＜0.05);(3)IRI后A组肾组织匀浆SOD活力高于B组(P＜0.05),A组肾组织匀浆MDA含量测定值低于B组,差异有统计学意义(P＜0.05).结论 建立的模型要求条件简单、易行,可用于肾移植冷缺血再灌注损伤相关的研究;

Abstract：

Objective In this study,for studying IRI in kidney transplantation. ,we established the models of cold ischemia and reperfusion injury in rats. Methods Twenty four SD rats were randomly assigned to two groups:control (A) ,and experimental (B) group. Group A was only removed the right kidney. Cold ischemia reperfusion was performed as the follow-listed model in Group B. The main process of the model: ( 1) Perfusing left kidney: after resected the right kidney of the rat, one pipe was put in the remainder right renal artery to perfuse the left kidney. The perfusion flowed out through another pipe in the right renal vein. The blood vessels of left kidney were clipped after cold perfusion. (2) Cold ischemic conservancy : the operation table was leant to left side, and the left kidney was taken out of abdominal cavity then stored in a cold bag which was full of ice and water,but the vessels of that were intact. (3) Reperfusing left kidney: after 60 minutes, the clip was removed. Left kidneys of all rats in two groups were removed to be detected. Structure of the kidney was evaluated by light microscopy and electronic microscopy. Superoxide dismutase ( SOD) activity and malondialdehyde ( MDA) content in the renal tissues was examined,and the renal function was also assessed by determining the levels of blood urea nitrogen ( BUN) and serum creatinine (CR) before and 24 hours after operation. Results (1) Morphologic change (hematoxylin-eosin staining) :A normal morphology was observed by light microscopy and electon microscopy in group A.Significant injury was detected in group B. (2 ) In group A, there was not significant difference about BUN and CR between before and after operation (P ＞0. 05) ,but in Group B,those increased significantly at 24 hour after operation (P ＜0. 05). (3) Activity of SOD in renal tissues in group A was higher than those in group B (P ＜ 0. 05 ) , meanwhile, Content of MDA in group A was lower than those in group B ( P ＜0. 05 ).Conclusion The rat renal cold ischemia reperfusion model we established is feasible regardless of experimental conditions, and can be studied as the events following IRI in kidney transplantation.     

Ozone administration reduces reperfusion injury in an isolated rat heart model

BACKGROUND: Accumulating clinical experience with ozone administration for conditions associated with ischemia has been encouraging. The aim of our study was to determine the effect of ozone on reperfusion injury in an isolated rat heart model. METHODS: Isolated rat hearts were perfused with modified Krebs-Henseleit buffer solution via ascending aorta cannulation. After 15 minutes, perfusion was stopped and global ischemia was maintained for 30 minutes, following which perfusion was restarted, and continued for 40 minutes. Baseline hemodynamic measurements (heart rate, left ventricular developed pressure (LVDP), dP/dt, and coronary flow) were taken prior to ischemia, and every 10 minutes after reperfusion was started. Eleven hearts were treated with ozone during reperfusion and eight hearts served as controls. In the treatment group, after 5 minutes of reperfusion, ozone was administered in distilled water via a side arm for 5 minutes. RESULTS: Preischemic baseline hemodynamic measurements and coronary flow were similar in the two groups. Hearts treated with ozone during reperfusion exhibited better recovery than did controls. Mean (+/-SE) percent recovery for treatment and control groups, respectively, was: LVDP 69 +/- 2% vs 51 +/- 6% (p = 0.04); dP/dt 68.9 +/- 13.3% vs 53.7 +/- 20.4% (p = 0.05); and LVDPxHR 61.4 +/- 3.3% vs 44.4 +/- 3.5% (p = 0.02). CONCLUSION: In the isolated rat heart model, treatment with ozone during reperfusion enables better recovery than in controls. Although the mechanism by which ozone exerts its beneficial effect is not identified, it is possibly due to reduction in reperfusion injury.     

高渗灌注对大鼠心肌缺血-再灌注损伤的影响

目的在Langendorff灌注模型上研究高渗灌注对大鼠心肌缺血-再灌注损伤耐受性的影响。方法健康雄性SD大鼠20只,随机分为对照组(C组)和高渗氯化钠灌注组(H组),每组10只。腹腔注射戊巴比妥钠(60mg/kg)麻醉后快速取出心脏接上主动脉插管置于Langendorff装置上,Krebs-Henseleit缓冲液平衡逆行灌注20min。待HR及冠脉流量平稳后夹闭灌注道进行全心热缺血30min,复灌40min。通过多道生理记录仪持续监测HR、左心室压峰值(LVPSP)、左室舒张末压(LVEDP)和左室压力最大上升/下降速率(±dp/dtmax),计算左室发展压(LVDP=LVPSP-LVEDP),用左室发展压与心率乘积(RPP=LVDP×HR)表示左室做功。结果同C组比较,H组再灌注心功能恢复显著改善:HR[(89.5±7.8)%vs(57.9±4.6)%,P<0.05]、LVPSP[(83.5±7.8)%vs(62.9±4.1)%,P<0·05]、RPP[(66.3±9.4)%vs(36.4±3.8)%,P<0.05]、冠脉流量(CF)[(61.2±8.9)%vs(41.9±4.0)%,P<0.05]、+dp/dtmax[(60.4±6.9)%vs(22.9±3.4)%,P<0.01]和-dp/dtmax[(69.5±6.6)%vs(34.3±3.3)%,P<0.01];肌酸激酶(CK)释放量显著降低(P<0.05)。结论高渗灌注减轻心肌缺血-再灌注损伤。     

左西孟旦乌司他丁与其联合用药对幼兔离体心脏的保护作用

Objective Levosimendan,a new calcium ion sensitizer,is currently used in the treatment of heart failure and as an option for patients with injury to the left heart or at high risk for surgery.The study tried to evaluate the effects of levosimendan and ulinastain for protecting myocardium from ischemia-reperfusion (I/R) injury to the isolated immature rabbit hearts and investigate the possible mechanism.Methods Fifty New Zealand long-ear white immature rabbits were anesthetized and heparinized.Their hearts were rapidly removed and mounted on modified Langendorff apparatus.A left ventricle pressure monitoring line was inserted through the left atrial and mitral valve.The hearts were equilibrated with oxygenated K-H solution at 37℃ for 10 minutes.The rabbit hearts were randomly divided into 5 groups with 10 hearts in each group.Hearts in group C were perfused with K-H solution,in group U were perfused with ulinastain (50000 U/kg),in group LI were perfused with Levosimendan 0.1 μmol/L,in group L2 were perfused with Levosimendan 0.3 μmol/L,and in group L + U were perfused with Ulinastain (50 000 U/kg) and Levosimendan 0.1μmol/L.The hearts were arrested with St-Thomas solution for 30 min.Hearts in each group underwent 30 min-reperfusion with the same solutions after 30 min-global myocardial ischemia.Heart rate ( HR) Jeft ventricular pressure ( LVP) and LVdp/dtMax were monitored.Effluent from coronary sinus was collected at time of ischemia /reperfusion for measuring the concentration of TNF-α,IL-6,CK and cTnI.Results LVP and LVdp/dt in group L1,L2 and L + U were better than those in group C and U.But the heart rates in group L2 were higher than in other groups.Concentrations of CK,cTnI,TNF-α and IL-6 in the effluent from coronary sinus at 0、10 and 30 min of reperfusion were significantly lower in group L + U than in the other groups.Conclusion Levosimendan may have the similar effects with ulinastain in reducing the reperfusion injury to the immature myocardium.The protective effect of levosimendan (0.1 μmol/L) in combination with ulinastain (50 000 U/kg) was better than that of levosimendan or ulinastain alone.     

左西孟旦乌司他丁与其联合用药对幼兔离体心脏的保护作用

Objective Levosimendan,a new calcium ion sensitizer,is currently used in the treatment of heart failure and as an option for patients with injury to the left heart or at high risk for surgery.The study tried to evaluate the effects of levosimendan and ulinastain for protecting myocardium from ischemia-reperfusion (I/R) injury to the isolated immature rabbit hearts and investigate the possible mechanism.Methods Fifty New Zealand long-ear white immature rabbits were anesthetized and heparinized.Their hearts were rapidly removed and mounted on modified Langendorff apparatus.A left ventricle pressure monitoring line was inserted through the left atrial and mitral valve.The hearts were equilibrated with oxygenated K-H solution at 37℃ for 10 minutes.The rabbit hearts were randomly divided into 5 groups with 10 hearts in each group.Hearts in group C were perfused with K-H solution,in group U were perfused with ulinastain (50000 U/kg),in group LI were perfused with Levosimendan 0.1 μmol/L,in group L2 were perfused with Levosimendan 0.3 μmol/L,and in group L + U were perfused with Ulinastain (50 000 U/kg) and Levosimendan 0.1μmol/L.The hearts were arrested with St-Thomas solution for 30 min.Hearts in each group underwent 30 min-reperfusion with the same solutions after 30 min-global myocardial ischemia.Heart rate ( HR) Jeft ventricular pressure ( LVP) and LVdp/dtMax were monitored.Effluent from coronary sinus was collected at time of ischemia /reperfusion for measuring the concentration of TNF-α,IL-6,CK and cTnI.Results LVP and LVdp/dt in group L1,L2 and L + U were better than those in group C and U.But the heart rates in group L2 were higher than in other groups.Concentrations of CK,cTnI,TNF-α and IL-6 in the effluent from coronary sinus at 0、10 and 30 min of reperfusion were significantly lower in group L + U than in the other groups.Conclusion Levosimendan may have the similar effects with ulinastain in reducing the reperfusion injury to the immature myocardium.The protective effect of levosimendan (0.1 μmol/L) in combination with ulinastain (50 000 U/kg) was better than that of levosimendan or ulinastain alone.     

The effect of controlled reperfusion in porcine hearts submitted to three hours of cold global ischemia

Abstract. At present, many investigations of myocardial function following ischemic insults concentrate on the modalities of reperfusion rather than on the mode of preservation. In this study, we tried to define the effect of reperfusion using warm blood cardioplegia (WBC) after medium-term (3 h) cold global ischemia, as required in cardiac transplantation. Twenty-one porcine hearts were harvested after preservation with cold cardioplegia (St. Thomas Hospital solution) and topical cooling. Normothermic reperfusion with blood was initiated after 3 h of ischemia utilizing a special extracorporeal pump circuit. Twelve hearts served as controls (group A), while substrate-enriched WBC was applied during the initial 20 min of reperfusion in nine hearts (group B). Hearts in both groups were then studied for myocardial function and metabolism under both working and nonworking conditions for a maximum of 180 min. In the nonworking mode, left ventricular dp/dt was significantly higher in group B than in group A at 15 min (2201 ± 785 mm Hg/sec vs 1515 ± 732 mm Hg/sec) and at 180min (1730 ± 471 mm Hg/sec vs 836 ± 147 mm Hg/sec; P <0. 05). After 3 h, lactate production was significantly higher in group A (371 ± 45mg/dl) than in group B (108 ± 44 mg/dl; P < 0. 05). Creatine kinase release into the coronary sinus was also significantly elevated in group A at-15min (2807 ± 1478 IU/l vs 1148 ± 1272 IU/l; P < 0. 05). Similarly, the hemodynamic data obtained under working conditions in group B were superior to those in group A. We conclude that following 3 h of cold global ischemia, reperfusion with WBC improves myocardial function and metabolism. Cautious application in clinical heart transplantation is recommended.     

The effect of controlled reperfusion in porcine hearts submitted to three hours of cold global ischemia

At present, many investigations of myocardial function following ischemic insults concentrate on the modalities of reperfusion rather than on the mode of preservation. In this study, we tried to define the effect of reperfusion using warm blood cardioplegia (WBC) after medium-term (3 h) cold global ischemia, as required in cardiac transplantation. Twenty-one porcine hearts were harvested after preservation with cold cardioplegia (St. Thomas Hospital solution) and topical cooling. Normothermic reperfusion with blood was initiated after 3 h of ischemia utilizing a special extracorporeal pump circuit. Twelve hearts served as controls (group A), while substrate-enriched WBC was applied during the initial 20 min of reperfusion in nine hearts (group B). Hearts in both groups were then studied for myocardial function and metabolism under both working and nonworking conditions for a maximum of 180 min. In the nonworking mode, left ventricular dp/dt was significantly higher in group B than in group A at 15 min (2201±785 mm Hg/sec vs 1515±732 mm Hg/sec) and at 180 min (1730±471 mm Hg/sec vs 836±147 mm Hg/sec;P<0.05). After 3 h, lactate production was significantly higher in group A (371±45 mg/dl) than in group B (108±44 mg/dl;P<0.05). Creatine kinase release into the coronary sinus was also significantly elevated in group A at 15 min (2807±1478 IU/l vs 1148±1272 IU/l;P<0.05). Similarly, the hemodynamic data obtained under working conditions in group B were superior to those in group A. We conclude that following 3 h of cold global ischemia, reperfusion with WBC improves myocardial function and metabolism. Cautious application in clinical heart transplantation is recommended.