体外循环中心肌细胞膜通透性变化的镧示踪研究

我们采用镧示踪法观察猫体外循环缺血 再灌注过程中心肌细胞膜通透性的变化 ,为探讨缺血再灌注损伤和恢复的膜分子机理及改进临床心肌保护措施提供依据。一、材料和方法1.动物分组 :健康猫 15 0只 ,体重( 3.0± 0 .5 )ｋｇ ,随机分为 6组 (组Ⅰ 15只 ,其余组各 2 7只 )。组Ⅰ仅作体外循环转流 ,不阻断主动脉 ;组Ⅱ主动脉阻断(ＡＣＣ)期间不行心肌保护 ;组Ⅲ、Ⅳ、Ⅴ中度低温体外循环 ,ＡＣＣ期间分别间断顺灌冷晶体、冷血心停搏液和持续顺灌冷血心停搏液 ;组Ⅵ常温体外循环 ,ＡＣＣ期间持续顺灌温血心停搏液。2 .建立体外循环模型 :按文献 …     

温血停搏液持续与间断灌注在冠状动脉搭桥术中的比较研究

目的 比较温血持续与间断灌注心脏停搏液在冠状动脉搭桥术中心肌保护效应。方法将30例冠状动脉搭桥手术随机分为温血持续灌注组（n=15）;温血间断灌注组（n=15）,灌注心脏停搏液,在常温体外循环下分别于切皮前、转流60min、停机6、12h采集动脉血,以ELISA法测定血浆心肌肌钙蛋白T（cTnT）浓度。分别取主动脉阻断前、开放后心肌组织,观察三磷酸腺苷（ATP）含量及心肌超微结构。结果 温血间断组 cTnT在停机6h时点比温血持续组有显著性差异（P<0.05）。两组术中60min、停机6hcTnT升高,停机24h逐渐恢复术前水平。两组ATP含量比主动脉阻断前有显著性差异（P<0.05）。温血间断组线粒体计分主动脉阻断开放后比主动脉阻断开放前有显著性差异（P<0.05）,温血持续组略升高（P<0.05）。结论 常温体外循环中温血持续灌注停搏液优于温血间断灌注停搏液的心肌保护作用。     

开放主动脉前灌注含甘露醇的温血停搏液对心肌MDA和SOD…

利用猫体外循环模型。观察心有缺血再灌注过程中ＭＤＡ，ＳＯＤ的变化，开放主动脉再灌注含甘露醇的温血停搏液对其影响。结果见缺血心肌再灌注后线粒体ＭＤＡ含量明显增，缺血心肌复灌前从主动脉根部注入含甘露醇温血停搏液，使心脏在有氧下停搏，可降低心肌线粒体ＭＤＡ含量，提高心肌ＳＯＤ活性，表明缺血心肌在恢复正常血供前灌注含甘露醇温血停搏液，可减轻膜脂质的过氧化，保护自由基清除系统，减轻心肌的再灌注损伤。     

常温体外循环下常温充氧晶体和氧合血停搏液持续灌注的心肌…

对比研究常温体外循环下常温充氧晶体和氧合血停搏液持续灌注对阻断升主动脉后犬心肌的保护效果，１５只犬随机分三组，每组５只，即低温体外循环冷搏液间断灌注组；常温体外循环常温氧合血停搏液持续灌注组；常温体外循环常温充氧晶掏搏液持续灌注组。观察了阻断升主动脉前心肌超微结构，腺苷酸含量（ＡＴＰ、ＡＤＰ、ＡＭＰ）、脂质过氧化物、水含量及血流动力学的变化。结果显示，温血组和温晶组在阻断升主动脉１５分钟、５０分钟     

开放主动脉前灌注含甘露醇的温血停搏液对心肌MDA和SOD的影响

利用猫体外循环模型，观察心肌缺血再灌注过程中ＭＤＡ、ＳＯＤ的变化，及开放主动脉前灌注含甘露醇的温血停搏液对其影响。结果见缺血心肌再灌注后线粒体ＭＤＡ含量明显增加；缺血心肌复灌前从主动脉根部注入含甘露醇温血停搏液，使心脏在有氧环境下停搏，可降低心肌线粒体ＭＤＡ含量，提高心肌ＳＯＤ活性。表明缺血心肌在恢复正常血供前灌注含甘露醇温血停搏液，可减轻膜脂质的过氧化，保护自由基清除系统，减轻心肌的再灌注损伤。     

温血间断停灌对心肌肌浆网摄钙功能的影响

目的　评价温血心脏停搏液不同间断灌注时程对心肌保护效果的影响。　方法　将４６ 只大鼠随机分为６组。组Ⅰ：温血心脏停搏液持续灌注;组Ⅱ：每２０ 分钟重复停灌５ 分钟;组Ⅲ：每２０ 分钟重复停灌１０ 分钟;组Ⅳ：停搏期一次停灌１０ 分钟;组Ⅴ：停搏期一次停灌１５ 分钟,以上每组８ 只大鼠;对照组：６ 只大鼠,心脏经Ｌａｎｇｅｎｄｏｒｆｆ 和工作心灌注各１０ 分钟后置液氮冻存。测定各组心功能,心肌肌浆网钙离子三磷酸腺苷酶（ＳＲ Ｃａ２ ＋ＡＴＰａｓｅ） 活性,心肌肌浆网４５Ｃａ２ ＋ 摄取和超微结构的改变。　结果　组Ⅱ心肌保护效果未受影响;组Ⅳ心功能恢复有影响,但心肌肌浆网泵功能保持正常;组Ⅲ和组Ⅴ心功能、心肌ＳＲ Ｃａ２ ＋ＡＴＰａｓｅ 活性和心肌肌浆网４５Ｃａ２ ＋ 摄取均有明显减退,超微结构亦受损。　结论　温血心脏停搏液间断停灌５ 分钟不影响其保护效果,一次或重复停灌１０ 分钟对心肌保护有负性作用,温血心脏停搏液停灌不宜超过１０ 分钟。     

温血心脏停搏液持续灌注对长时间停搏心肌的保护作用

目的利用猫体外循环模型对比观察间断冷血、持续冷血及持续温血心脏停搏液灌注对长时间停搏心肌的保护作用。方法健康猫２４只，随机分成４组：Ⅰ组为正常对照组，取正常猫心测定有关指标做为正常对照；Ⅱ～Ⅳ组为心脏停搏组，停搏时间３小时，用不同心肌保护方法保护心肌。结果心脏停搏３小时后心肌线粒体呼吸功能、氧化磷酸化能力及心肌三磷酸腺苷（ＡＴＰ）含量在间断冷血组明显下降，持续冷血组呈轻度下降，持续温血组保持正常。结论持续灌注温血停搏液技术可使心脏在停搏期间有充足的血液供应，是一种理想的心肌保护方法，特别适用于需长时间停搏和高危病例。     

温血停搏液术终灌注对缺血再灌注心肌的保护作用

利用猫体外循环模型观察含甘露醇的温血停搏液术终灌注对缺血再灌注心肌的保护作用。心肌缺血恢复正常血液灌注前，从主动脉根部以５～６ｋＰａ的压力注入３７℃含甘露醇的低钾温血停搏液５０ｍｌ。结果显示用含甘露醇的温血停搏液术终灌注可保护缺血后再灌注心肌的功能，提高心肌能量储备，降低线粒体丙二醛含量。结论：含甘露醇的温血停搏液术终灌注，可提高心肌对氧自由基的清除能力，减轻线粒体膜脂质过氧化，提高心肌能量储备，有利于再灌注后心肌功能的恢复     

顺逆灌结合开放前温血灌注在冠状动脉旁路移植术中的心肌保护作用

目的回顾研究顺逆灌结合开放前温血灌注在冠状动脉旁路移植术(CABG)中的心肌保护作用。方法择期CABG患者312例,男220例,女92例,年龄29~80岁(平均62岁);其中顺逆灌结合温血灌注188例(研究组),间断顺灌124例(对照组)。研究组采用顺行灌注2 min冷血停搏液600 ml,再逆行灌注2 min停搏液400 ml,之后每隔10 min进行顺逆灌各1 min停搏液200 ml,在开始吻合前降支时持续温血逆灌300 ml/min直至开放。记录搭桥数、心脏自动复跳率、CPB时间、主动脉阻断时间、机械通气时间、ICU停留时间、住院天数。结果研究组CPB时间、机械通气时间、住院天数明显短于对照组(P<0.05)。结论 CABG中采用顺逆灌结合开放前温血灌注的心肌保护效果优于常规间断顺灌方法,值得临床推广。     

氨基酸盐温血停搏液诱导和末次灌注对缺血犬心肌的保护作用

为研究氨基酸盐温血停搏液诱导和末次灌注对缺血犬心肌的保护作用,应用犬体外循环工作模型,心肌缺血120分钟。动物随机分为3组,Ⅰ组:温血停搏液诱导和末次灌注,中间用st.Thomas’NO.2液(STS)冷晶体停搏液;Ⅱ组同Ⅰ组,但诱导与末次灌注温血停搏液中含L—门冬氨酸(L-asperte,A)和L—谷氨酸钠(L-glutamate,G)各13mmol/L;Ⅲ组同Ⅱ组,但STS液中亦含相同浓度的氨基酸(AG)。结果表明,缺血复灌后,AG用于温血和冷晶体停搏液中(Ⅱ、Ⅲ组),心功能恢复明显改善,Ⅲ组在缺血后心肌ATP含量明显高于Ⅰ组(P<0.05)。心肌超微结构Ⅲ组缺血前后无明显改变。本实验提示:温血及冷停搏液中含AG进一步加强了心肌保护作用。     

Warm reperfusion and myocardial protection

Background. The aim of this study was to determine whether warm reperfusion improves myocardial protection with cardiac troponin I as the criteria for evaluating the adequacy of myocardial protection.

Methods. One hundred five patients undergoing first-time elective coronary bypass surgery were randomized to one of three cardioplegic strategies of either (1) cold crystalloid cardioplegia followed by warm reperfusion, (2) cold blood cardioplegia followed by warm reperfusion, or (3) cold blood cardioplegia with no reperfusion.

Results. The total amount of cardiac troponin I released tended to be higher in the cold blood cardioplegia with no reperfusion group (3.9 ± 5.7 μg) than in the cold blood cardioplegia followed by warm reperfusion group (2.8 ± 2.7 μg) or the cold crystalloid cardioplegia followed by warm reperfusion group (2.8 ± 2.2 μg), but not significantly so. Cardiac troponin I concentration did not differ for any sample in any of the three groups.

Conclusions. Our study showed that the addition of warm reperfusion to cold blood cardioplegia offers no advantage in a low-risk patient group.     

Warm induction cardioplegia and reperfusion dose influence the occurrence of the post CABG TnI level

As a new biochemical marker cardiac troponin-I (CTnI) is a more sensitive and specific marker for detection of differences in myocardium injuries than other chemical enzymes. This study investigates the effect of warm induced and reperfusion blood cardioplegia on the release of troponin-I during the CABG. In our research, 24 three-vessel coronary artery disease (CAD) patients underwent CABG and were divided into two groups randomly: Group of warm induction and reperfusion blood cardioplegia (Group W N=12); Group of simple warm induction and no reperfusion (Group C N=12). The effect of myocardium protection of the two methods of myocardium protection were evaluated by clinical outcome, CTnI. Serial venous blood samples were obtained before and after surgery. In both groups, there were no differences in operative parameters. The level of CTnI increased from postoperative 6 h (P<0.05), reached peak in 24 approximately 72 h and recovered postoperatively on 6th day in both groups. Compared with group C, the plasma concentrations of CTnI in group W were significantly lower at 6 h, 24 h and 72 h (P<0.01). The results suggest that the method of warm induction and reperfusion blood cardioplegia reduces the leakage of CTnI than group of simple warm blood cardioplegia in CABG patients.     

Effects of supplemental L-arginine during warm blood cardioplegia.

OBJECTIVES: Effects of supplemental L-arginine, nitric oxide precursor, during warm blood cardioplegia were assessed in the blood perfused isolated rat heart. METHODS: The isolated hearts were perfused with blood at 37 degrees C from a support rat. After 20 minutes of aerobic perfusion, the hearts were arrested for 60 minutes with warm blood cardioplegia given at 20-minute intervals. This was followed by 60 minutes of reperfusion. The hearts were divided into the following three groups according to the supplemental drugs added to the cardioplegic solution. The control group (n = 10) received standard warm blood cardioplegia. The L-ARG group (n = 10) received warm blood cardioplegia supplemented with L-arginine (3 mmol/l). The L-NAME group (n = 10) received warm blood cardioplegia supplemented with L-arginine (3 mmol/l) and L-nitro-arginine methyl ester, a competitive inhibitor of nitric oxide synthase (1 mmol/l). After 60 minutes of cardioplegic arrest, cardiac function, myocardial metabolism and myocardial release of circulating adhesion molecules were measured during reperfusion. RESULTS: Left ventricular end-diastolic pressure was significantly lower (p<0.05) in the L-ARG group than in the control group and the L-NAME group during reperfusion. Isovolumic left ventricular developed pressure, dp/dt and coronary blood flow were significantly greater (p< 0.05) in the L-ARG group during reperfusion. The L-ARG group resulted in early recovery of lactate metabolism during reperfusion. Myocardial release of circulating intercellular adhesion molecule-1 (ICAM-1) and E-selectin were significantly less (p<0.05) in the L-ARG group at 15 minutes of reperfusion. CONCLUSIONS: The results suggest that augmented nitric oxide by adding L-arginine to warm blood cardioplegia can preserve left ventricular function and ameliorate endothelial inflammation. The technique can be a novel cardioprotective strategy in patients undergoing cardiac surgery.     

Intermittent antegrade hyperkalaemic warm blood cardioplegia supplemented with magnesium prevents myocardial substrate derangement in patients undergoing coronary artery bypass surgery

Objective: The influence of the addition of magnesium on myocardial protection with intermittent antegrade warm blood hyperkalaemic cardioplegia in patients undergoing coronary artery surgery was investigated and compared with intermittent antegrade warm blood hyperkalaemic cardioplegia only. Methods: Twenty-three patients undergoing primary elective coronary revascularization were randomized to one of two different techniques of myocardial protection. In the first group, myocardial protection was induced using intermittent antegrade warm blood hyperkalaemic cardioplegia. In the second group, the same technique was used except that magnesium was added to the cardioplegia. Intracellular substrates (ATP, lactate and amino acids) were measured in left ventricular biopsies collected 5 min after institution of cardiopulmonary bypass, after 30 min of ischaemic arrest and 20 min after reperfusion. Results: There were no significant changes in the intracellular concentration of ATP or free amino acid pool in biopsies taken at the end of the period of myocardial ischaemia. However, the addition of magnesium prevented the significant increase in the intracellular concentration of lactate seen with intermittent antegrade warm blood hyperkalaemic cardioplegia. Upon reperfusion there was a significant fall in ATP and amino acid concentration when the technique of intermittent antegrade warm blood hyperkalaemic cardioplegia was used but not when magnesium was added to the cardioplegia. Conclusions: This work shows that intermittent antegrade warm blood hyperkalaemic cardioplegia supplemented with magnesium prevents substrate derangement early after reperfusion.     

Intermittent warm blood cardioplegia induces the expression of heat shock protein-72 by ischemic myocardial preconditioning

OBJECTIVE: Recent studies have demonstrated that the induction of heat shock protein-72 (HSP72) by different stimuli preserves the heart function after cardioplegic arrest. Based on these findings, we investigated whether intermittent warm blood cardioplegia would induce changes in the myocardial expression of HSP72. METHODS: Forty patients scheduled for aortocoronary bypass were randomly assigned to receive either cold or warm intermittent blood cardioplegia. In all patients HSP72 and HSP72 mRNA were assayed in biopsies from the right atrium at baseline, and during the reperfusion period. Plasma CK-MB and troponin-T, and myocardial oxygen extraction and lactate release were also measured. RESULTS: In both groups, myocardial expression of HSP72 increased throughout the reperfusion period, but the values of HSP72 band lengths were significantly higher in the warm group. Correspondingly, HSP72 mRNA levels increased progressively in both groups, with significant difference between groups observed in biopsies at the reperfusion. Warm blood cardioplegia was associated with lower levels of CK-MB and troponin-T. Myocardial oxygen extraction and lactate release were higher during intermittent warm cardioplegia, indicating a more profound ischemic anaerobic metabolism in the warm group. CONCLUSIONS: Intermittent warm blood cardioplegia induces an increased expression of HSP72 and it is associated with a better myocardial protection, by a mechanism involving a variant of the classical ischemic preconditioning model.     

Terminal Warm Blood Cardioplegia Improves Cardiac Function Through Microtubule Repolymerization

Background. To elucidate the mechanisms responsible for the beneficial effects of terminal warm blood cardioplegia, we studied dynamic change in microtubules induced by cold cardioplegia followed by rewarming. Further, we investigated the relationship between cardiac function and morphologic changes in microtubules caused by hyperkalemic, hypocalcemic warm cardioplegia during initial reperfusion.

Methods. In protocol 1 isolated rat hearts were perfused at 37°C with Krebs-Henseleit buffer (KHB). After 3 hours of hypothermic cardiac arrest at 10°C, hearts were reperfused at 37°C with one of two buffers: group C, 60-minute reperfusion with KHB (K⁺, 5.9 mmol/L; Ca²⁺, 2.5 mmol/L); and group TC, 10-minute initial reperfusion with modified KHB (K⁺, 15 mmol/L; Ca²⁺, 0.25 mmol/L), followed by 50 minutes of reperfusion with KHB. Cardiac function after reperfusion was determined as a percentage of the prearrest value. In protocol 2 hearts were perfused at 37°C with KHB containing colchicine (10⁻⁵ mol/L) for 60 minutes.

Results. There was spontaneous contractile recovery after 10 minutes of initial reperfusion in hearts from group TC as well as improved cardiac function after 15, 30, and 60 minutes of reperfusion compared with that in group C. Immunohistochemical staining and immunoblot analysis demonstrated microtubule depolymerization during hypothermic cardiac arrest and complete repolymerization after 10 minutes of reperfusion with warm buffers in both groups. Colchicine-induced microtubule depolymerization is associated with deterioration of cardiac function.

Conclusions. One mechanism responsible for improved cardiac function mediated by terminal warm blood cardioplegia is the restart of contraction after complete microtubule repolymerization.     

Effects of angiotensin-converting enzyme inhibitor during warm blood cardioplegia

BACKGROUND: Effects of captopril, an angiotensin-converting enzyme inhibitor, during warm blood cardioplegia were assessed in the blood-perfused, isolated rat heart. METHODS: The isolated hearts were arrested for 60 minutes with warm blood cardioplegia given at 20-minute intervals and were reperfused for 60 minutes. The control group (n = 10) received standard cardioplegia and the captopril group (n = 10) received cardioplegia supplemented with captopril (2 mmol/L). Cardiac function, myocardial metabolism, and cardiac release of circulating adhesion molecules were assessed before and after cardioplegic arrest. RESULTS: Left ventricular end-diastolic pressure and -dp/dt were significantly (p<0.05) lower and coronary blood flow was significantly (p<0.05) greater in the captopril group than the control group during reperfusion. The captopril group resulted in significantly (p<0.05) less cardiac release of lactate, thiobarbituric acid reactive substances during reperfusion. Cardiac release of intercellular adhesion molecule-1 was significantly (p<0.05) less in the captopril group at 60 minutes of reperfusion. CONCLUSIONS: The results suggest that supplementation of captopril during warm blood cardioplegia provides superior myocardial protection by suppressing lipid peroxidation and leukocyte-endothelial cell interaction during reperfusion.     

Blood warm reperfusion: a necessary adjunct to heart-valve surgery in low-risk patients?

AIM: The aim of this prospective, randomized study was to determine whether blood warm reperfusion improves myocardial protection provided by cold crystalloid cardioplegia in patients undergoing first-time elective heart-valve surgery, using cardiac troponin I release as the criterion for evaluating the adequacy of myocardial protection. METHODS: Seventy patients with a left ventricular ejection fraction greater than 40% were randomly assigned to 1 of 2 myocardial protection strategies: 1) cold crystalloid cardioplegia with no reperfusion or 2) cold crystalloid cardioplegia followed by 2-minute blood warm reperfusion before aortic unclamping. Cardiac troponin I concentrations were measured in serial venous blood samples drawn immediately prior to cardiopulmonary bypass and after aortic unclamping at 6, 9, 12, and 24 h. RESULTS: Randomization produced 2 equivalent groups. The total amount of cardiac troponin I released (7.17+/- 14.8 mg in the crystalloid cardioplegia with no reperfusion group and 5.82+/-4.66 mg in the crystalloid cardioplegia followed by blood warm reperfusion group) was not different (P > 0.2). Cardiac troponin I concentration did not differ for any sample in either of the 2 groups. The total amount of cardiac troponin I released was higher in patients who required inotropic support (9.14 +/-16.2 mg) than those who did not (4.73+/-4.52 mg; P = 0.009). CONCLUSIONS: Our study shows that adding blood warm reperfusion to cold crystalloid cardioplegia provides no additional myocardial protection in low-risk patients undergoing heart-valve surgery.     

Cardioprotective effects and the mechanisms of terminal warm blood cardioplegia in pediatric cardiac surgery

OBJECTIVES: Terminal warm blood cardioplegia has been shown to enhance myocardial protection in adult patients. However, the cardioprotective effects and the mechanisms of terminal warm blood cardioplegia in pediatric heart surgery were still unknown. METHODS: One hundred three consecutive patients were prospectively randomized to one of two groups. In the control group (n = 52), myocardial protection was achieved with intermittent hyperkalemic cold blood cardioplegia and topical cardiac cooling. In the terminal warm blood cardioplegia group (n = 51), this was supplemented with terminal warm blood cardioplegia before the aorta was declamped. Arterial and coronary sinus blood samples were analyzed to determine myocardial energy metabolism and tissue injury. RESULTS: There were no significant differences between the two groups in age (5.5 +/- 0.6 years in the control group vs 5.6 +/- 0.5 years in the terminal warm blood cardioplegia group), body weight (17.2 +/- 1.4 kg in the control group vs 19.8 +/- 1.7 kg in the terminal warm blood cardioplegia group), percentage of cyanotic heart diseases (50% in the control group vs 51% in the terminal warm blood cardioplegia group), number of patients who required right ventriculotomy (33% in the control group vs 39% in the terminal warm blood cardioplegia group), cardiopulmonary bypass time (194 +/- 12.1 minutes in the control group vs 177 +/- 8.6 minutes in the terminal warm blood cardioplegia group), aortic crossclamp time (83.3 +/- 5.9 minutes in the control group vs 82.3 +/- 5 minutes in the terminal warm blood cardioplegia group), lowest rectal temperature (27.4 +/- 0.3 degrees C in the control group vs 28.1 +/- 0.3 degrees C in the terminal warm blood cardioplegia group), and myocardial temperature (9.6 +/- 0.6 degrees C in the control group vs 9.6 +/- 0.7 degrees C in the terminal warm blood cardioplegia group). Spontaneous defibrillation occurred after reperfusion in 80% in the terminal warm blood cardioplegia group, which was significantly (P <.05) higher than the control group (62%). The lactate extraction rate at 60 minutes of reperfusion was significantly (P <.05) higher in the terminal warm blood cardioplegia group (9.0 +/- 2.8%) than the control group (-3.3 +/- 2.4%). The postreperfusion values of cardiac troponin T (7.4 +/- 0.6 ng/mL vs 11.2 +/- 1.0 ng/mL at 6 hours; 4.6 +/- 0.6 ng/mL vs 9.3 +/- 1.6 ng/mL at 18 hours) and heart-type fatty acid binding protein (137 +/- 28 ng/mL vs 240 +/- 30 ng/mL at 2 hours; 88 +/- 19 ng/mL vs 162 +/- 26 ng/mL at 3 hours) were significantly (P <.05 vs the control group) lower in the terminal warm blood cardioplegia group. CONCLUSION: Terminal warm blood cardioplegia enhances myocardial protection in pediatric cardiac surgery by an improvement in aerobic energy metabolism and a reduction of myocardial injury or necrosis.     

Preconditioning during warm blood cardioplegia

Objective: Preconditioning describes the cardioprotective effects of multiple brief episodes of warm ischemia. The purpose of the study was to determine whether warm ischemia, during the intermittent delivery of warm blood cardioplegia, would induce preconditioning during cardioplegia arrest. Methods: Dogs, 15, were randomized to a preconditioning protocol or to serve as controls. The control group received 60 min of continuous warm blood cardioplegia (WBC) followed by 30 min of warm arrested ischemia. The preconditioned group were arrested with WBC and then underwent three consecutive cycles consisting of 10 min of warm ischemia followed by 10 min of reperfusion. Reperfusion was provided by a continuous infusion of WBC. The preconditioning protocol was followed by 30 min of warm arrested ischemia. Myocardial functional recovery was assessed before cardiopulmonary bypass and cardioplegia arrest and again 30, 60 and 90 min after the arrest. Pressure-volume loops were used to measure the maximum elastance of the left ventricle (E_max), diastolic compliance, and used to calculate preload recruitable stroke work area. Results: Myocardial functional recovery was better preserved after 30 min of warm arrested ischemia in those animals that had been preconditioned. Conclusion: Preconditioning may be induced when warm blood cardioplegia is delivered intermittently during cardioplegia arrest.