Warm or cold continuous blood cardioplegia provides similar myocardial protection.

BACKGROUND: This study was performed to investigate the effect of temperature of blood cardioplegia on the recovery of postischemic cardiac function. METHODS: Pigs on cardiopulmonary bypass were subjected to global ischemia (30 minutes), followed by cold (n = 10) or warm (n = 11) continuous antegrade blood cardioplegia (45 minutes) delivered at 55-60 mm Hg. RESULTS: Global left ventricular function, evaluated by preload recruitable stroke work, decreased with cold cardioplegia from 91 (85-103) [mean (quartile interval)], at baseline, to 73 (55-87) erg x 10(3)/mL postbypass (p = 0.03), but was unchanged after warm cardioplegia; 110 (80-132) to 109 (71-175) erg x 10(3)/mL (p > 0.5). However, the difference between treatment effects was not significant (p = 0.25). Diastolic function, evaluated by end-diastolic pressure-volume relation, deteriorated without any difference between groups. Mean cardioplegic flow was similar between groups. Coronary vascular resistance increased at constant rate during warm cardioplegic delivery, but remained unchanged with cold cardioplegia (p = 0.001 between regression coefficients). CONCLUSIONS: No significant difference was found in postischemic functional recovery comparing cold and warm continuous blood cardioplegia. Cold cardioplegia is therefore preferred due to added safety of hypothermia.     

Adenosine-enhanced ischemic preconditioning provides enhanced cardioprotection in the aged heart

Background. Recently we have reported a novel myoprotective protocol “adenosine-enhanced ischemic preconditioning” (APC), which extends and amends the protection afforded by ischemic preconditioning (IPC) by both reducing myocardial infarct size and enhancing postischemic functional recovery in the mature rabbit heart. However, the efficacy of APC in the senescent myocardium was unknown.

Methods. The efficacy of APC was investigated in senescent rabbit hearts and compared with magnesium-supplemented potassium cardioplegia (K/Mg) and IPC. Global ischemia (GI) hearts were subjected to 30 minutes of global ischemia and 120 minutes of reperfusion. Ischemic preconditioning hearts received 5 minutes of global ischemia and 5 minutes of reperfusion before global ischemia. Magnesium-supplemented potassium cardioplegia hearts received cardioplegia just before global ischemia. Adenosine-enhanced ischemic preconditioning hearts received a bolus injection of adenosine in concert with IPC. To separate the effects of adenosine from that of APC, a control group (ADO) received a bolus injection of adenosine 10 minutes before global ischemia.

Results. Infarct size was significantly decreased to 18.9% ± 2.7% with IPC (p < 0.05 versus GI); 17.0% ± 1.0% with ADO (p < 0.05 versus GI); 7.7% ± 1.3% with K/Mg (p < 0.05 versus GI, IPC, and ADO); and 2.1% ± 0.6% with APC (p < 0.05 versus GI, IPC, ADO, and K/Mg; not significant versus control). Only APC and K/Mg significantly enhanced postischemic functional recovery (not significant versus control).

Conclusions. Adenosine-enhanced ischemic preconditioning provides similar protection to K/Mg cardioplegia, significantly enhancing postischemic functional recovery and decreasing infarct size in the senescent myocardium.     

Protein kinase C isoform-dependent myocardial protection by ischemic preconditioning and potassium cardioplegia

OBJECTIVE: Ischemic preconditioning combined with potassium cardioplegia does not always confer additive myocardial protection. This study tested the hypothesis that the efficacy of ischemic preconditioning under potassium cardioplegia is dependent on protein kinase C isoform. METHODS: Isolated and crystalloid-perfused rat hearts underwent 5 cycles of 1 minute of ischemia and 5 minutes of reperfusion (low-grade ischemic preconditioning) or 3 cycles of 5 minutes of ischemia and 5 minutes of reperfusion (high-grade ischemic preconditioning) or time-matched continuous perfusion. These hearts received a further 5 minutes of infusion of normal buffer or oxygenated potassium cardioplegic solution. The isoform nonselective protein kinase C inhibitor chelerythrine (5 micromol/L) was administered throughout the preischemic period. All hearts underwent 35 minutes of normothermic global ischemia followed by 30 minutes of reperfusion. Isovolumic left ventricular function and creatine kinase release were measured as the end points of myocardial protection. Distribution of protein kinase C alpha, delta, and epsilon in the cytosol and the membrane fractions were analyzed by Western blotting and quantified by a densitometric assay. RESULTS: Low-grade ischemic preconditioning was almost as beneficial as potassium cardioplegia in improving functional recovery; left ventricular developed pressure 30 minutes after reperfusion was 70 +/- 15 mm Hg (P <.01) in low-grade ischemic preconditioning and 77 +/- 14 mm Hg (P <.001) in potassium cardioplegia compared with values found in unprotected control hearts (39 +/- 12 mm Hg). Creatine kinase release during reperfusion was also equally inhibited by low-grade ischemic preconditioning (18.2 +/- 10.6 IU/g dry weight, P <.05) and potassium cardioplegia (17.6 +/- 6.7 IU/g, P <.01) compared with control values. However, low-grade ischemic preconditioning in combination with potassium cardioplegia conferred no significant additional myocardial protection; left ventricular developed pressure was 80 +/- 17 mm Hg, and creatine kinase release was 14.8 +/- 11.0 IU/g. In contrast, high-grade ischemic preconditioning with potassium cardioplegia conferred better myocardial protection than potassium cardioplegia alone; left ventricular developed pressure was 121 +/- 16 mm Hg (P <.001), and creatine kinase release was 8.3 +/- 5.8 IU/g (P <.05). Chelerythrine itself had no significant effect on functional recovery and creatine kinase release in the control hearts, but it did inhibit the salutary effects not only of low-grade and high-grade ischemic preconditioning but also those of potassium cardioplegia. Low-grade ischemic preconditioning and potassium cardioplegia enhanced translocation of protein kinase C alpha to the membrane, whereas high-grade ischemic preconditioning also enhanced translocation of protein kinase C delta and epsilon. Chelerythrine inhibited translocation of all 3 protein kinase C isoforms. CONCLUSIONS: These results suggest that myocardial protection by low-grade ischemic preconditioning and potassium cardioplegia are mediated through enhanced translocation of protein kinase C alpha to the membrane. It is therefore suggested that activation of the novel protein kinase C isoforms is necessary to potentiate myocardial protection under potassium cardioplegia.     

Nicorandil pretreatment and improved myocardial protection during cold blood cardioplegia.

OBJECTIVE: The present study was designed to assess whether pretreatment with nicorandil enhanced myocardial protection provided by cold (15 degrees C) high-potassium (25 mmol/l) blood cardioplegia during open heart surgery. METHODS: Subjects were 40 patients with a variety of acquired heart diseases undergoing cardiac surgery involved cardiopulmonary bypass. They were randomly divided into two groups, 25 pretreated nicorandil (0.3 mg/kg) 30 minutes before aortic cross clamping, 15 not pretreated. After aortic cross clamping, the initial dose of cardioplegic solution (10 ml/kg) was administered through the ascending aorta and supplemental doses of cardioplegia (5 ml/kg) given each 30 minutes thereafter. Preoperative and postoperative cardiac troponin-T, myosin light chain 1 and cardiac enzymes were measured and hemodynamic data recorded. RESULTS: Postoperative serum creatine kinase and myosin light chain 1 were significantly lower in the nicorandil pretreatment group than in controls. Serum glutamic oxalacetic transaminase and troponin-T were lower and cardiac output was higher after surgery in the nicorandil group, although not statistically significant. CONCLUSION: This data suggests that pretreatment with nicorandil enhances the myocardial protection achieved by cold blood cardioplegia.     

The effectiveness of ischemic preconditioning on myocardial protection and comparison with K(+) cardioplegia

The purpose of this study is to investigate the effects of ischemic preconditioning on myocardial protection and to compare this method to K(+) crystalloid cardioplegia. Langendorff perfused isolated working rat hearts were used in the following groups. After 20 min of stabilisation, 30 hearts were divided into three groups. In group I (control, n=10), hearts were arrested with cold (+4 degrees C) Krebs-Henseleit (K-H) solution, in group II (cardioplegia, n=10) hearts were arrested with cold K(+) cardioplegia solution, and in group III (preconditioning, n=10) hearts were subjected to 5 min normothermic ischemia followed by 5 min reperfusion then arrested with cold K-H solution. All hearts were subjected to 30 min of global ischemia (24 degrees C) and 40 min of reperfusion. Hemodynamic measurements were performed with a left ventricular latex balloon using a data acquisition system. Creatine kinase (CK-MB) washout and Troponin I (cTnI) levels were determined from the coronary effluents. There was no significant difference among the three groups in any of the parameters (hemodynamic and biochemical) measured at the end of stabilisation period. During reperfusion, functional recovery and coronary flow were significantly improved in K(+) cardioplegia and preconditioned groups compared with control group. CK-MB washout and cTnI levels were significantly lower in groups II and III compared with group I at the reperfusion. However no significant difference was observed between K(+) cardioplegia and preconditioned groups among biochemical and hemodynamic parameters and coronary flow at the post-ischemic period. In conclusion, ischemic preconditioning is as effective as K(+) cardioplegia on myocardial protection and recovery of myocardial function during reperfusion.     

Continuous cold blood cardioplegia improves myocardial protection: a prospective randomized study

BACKGROUND: To assess the influence on myocardial protection of the rate of infusion (continuous vs intermittent) of cold blood cardioplegia administered retrogradely during prolonged aortic cross-clamping. The end-points were ventricular performance and biochemical markers of ischemia. METHODS: Seventy patients undergoing myocardial revascularization for three-vessel disease were prospectively randomized to receive intermittent or continuous retrograde cold blood cardioplegia. Hemodynamic measurements were obtained using a rapid-response thermodilution catheter and included right ventricular ejection fraction, cardiac output, left and right ventricular stroke work index, and systemic and pulmonary vascular resistance. Blood samples were obtained from the coronary sinus before cross-clamp application and immediately after cross-clamp removal for determinations of lactate and hypoxanthine. RESULTS: The left ventricular stroke work index trend was significantly superior (p = 0.038) by repeated-measures analysis in continuous cardioplegia. Other hemodynamic measurements revealed a similar trend. The need for postoperative inotropic drugs support was reduced in continuous cardioplegia. The release of lactate in the coronary sinus after unclamping was 2.30 +/- 0.12 mmol/L after intermittent cardioplegia and 1.97 +/- 0.09 mmol/L after continuous cardioplegia (p = 0.036). The release of hypoxanthine was 20.47 +/- 2.74 micromol/L in intermittent cardioplegia and 11.77 +/- 0.69 micromol/L in continuous cardioplegia (p = 0.002). CONCLUSIONS: Continuous cold blood cardioplegia results in improved ventricular performance and reduced myocardial ischemia in comparison with intermittent administration.     

Multicentre investigation of myocardial protection with cold cardioplegia

In order to analyze factors of importance for the efficiency of myocardial protection during open-heart surgery, a study was made of 144 patients undergoing isolated aortic valve replacement with various cardioplegic techniques. The cardioplegia was of Bretschneider type in 54 cases, St Thomas in 31 and Ringer-potassium type in 11 cases. Single or multi-dose blood cardioplegia was used in 11 cases and continuous blood cardioplegia in 30 cases. Local cardiac hypothermia was additionally employed in all patients. The efficiency of myocardial protection was assessed mainly from the incidence of postoperative conduction disturbances, myocardial enzyme release and need for inotropic support. All patients survived the operation. In 20% surgery was followed by transient or persistent disturbance of conduction, in 9% by abnormally increased CK-MB release and in 5% by requirement for inotropic support. Preoperative risk factors such as high age or severe left ventricular (LV) hypertrophy or dysfunction had little influence on the results. Patients in whom aortic stenosis (AS) was dominant in the complex with aortic insufficiency (AS + AI) showed 20-hour postoperative CK-MB enzyme activity twice as high as those with pure aortic insufficiency. The most important factors in myocardial protection were the duration of aortic occlusion and the myocardial temperature during cardioplegia. When the aortic occlusion lasted more than 80 min there was a 32% incidence of conduction disturbances and 20-hour CK-MB activity thrice as high as after shorter occlusion. Patients with mean myocardial temperature below 18 degrees C during cardioplegia invariably had low enzyme activities, which indicated good myocardial protection. The best overall results were obtained in patients operated on during hypothermia at 25-27 degrees C, with single or multi-dose blood cardioplegia and with efficient local cooling of the heart.     

缺血预处理与温-冷-温技术在冠状动脉旁路移植术中对心肌的保护作用

目的通过监测血浆肌酸激酶同工酶(CK-MB)、心肌肌钙蛋白I(cTnI) 的水平,评价三种不同的心肌保护方法在冠状动脉旁路移植术(CABG)中的应用. 方法将36例均为稳定型心绞痛、3支血管病变、首次施行CABG患者随机分成3组缺血预处理组、温血组、对照组, 观察临床结果和术后应用血管活性药情况,并于转流前、术毕、术后6～12 、24 、72小时和第6天分别抽静脉血测定 CK-MB、cTnI. 结果缺血预处理组和温血组的自动复跳率均为100%,明显高于对照组(58%); cTnI 和CK-MB的水平从术后6～12小时开始升高(P<0.05),在24小时达到峰值,在术后第6天恢复.与对照组比较缺血预处理组和温血组在术后6～12、24、72小时时cTnI 和CK-MB的水平明显低(P<0.01). 结论多次短时间的缺血预处理和"温-冷-温"技术在低危CABG患者中较常规方法更有利于对缺血心肌的保护.     

A comparison between ischemic preconditioning,intermittent cross-clamp fibrillation and cold crystalloid cardioplegia for myocardial protection during coronary artery bypass graft surgery

The aim of this study was to compare ischemic preconditioning (IPC) with two established methods of myocardial protection, namely cold crystalloid cardioplegia and intermittent cross-clamp fibrillation (ICCF), in coronary artery bypass graft (CABG) surgery. This was a prospective randomised study. Thirty CABG patients were randomised to receive: (a) St Thomas' cardioplegia solution no. 2; (b) ICCF; or (c) IPC (two 3-min periods of ischemia with 2-min of reperfusion). Surgery was performed under standardised conditions by one surgeon (WBP). The primary endpoint was cardiac troponin T release during the first 72 h after surgery. Mean troponin T at 72 h was significantly lower in the IPC group (0.5 microg/l; p=0.05, ANOVA) compared with the cardioplegia and ICCF groups (2.1 and 1.3 microg/l respectively). This suggests that ischemic preconditioning is superior at limiting myocardial necrosis during CABG, but there is no difference between cold crystalloid cardioplegia and intermittent cross-clamp fibrillation.     

Influence of ischemic preconditioning and blood cardioplegia protection on postischemic endothelial activation in coronary bypass surgery

Summary Background Hypothermic ischemia in open heart surgery and cardiopulmonary bypass involve a postischemic in-flammatory reaction caused by an activation of leukocytes and endothelia with the systemic release of cytokines and adhesion molecules. The present study addresses the question, if an amelioration of postischemic endothelial activation in the heart could be achieved by means of cardioplegic protection or ischemic preconditioning. In a randomized prospective study patients underwent a normothermic preconditioning procedure either followed by crystalloid or blood cardioplegia during coronary bypass surgery. Methods Patients (n=28) were included and randomized in the study according to defined criteria: Group A received St. Thomas cardioplegia, group B cold blood cardioplegia. Ischemic precon-ditioning was performed twice at normothermia under a cardiopulmonary bypass (CPB) for 5 min followed by 10 min of reperfusion before coronary aortic bypass graft (CABG) using St. Thomas (group C) or blood cardioplegia (group D) hypothermic protection. In coronary sinus blood and arterial blood myocardial (creatine-kinase myoglobin [CK-MB]) and endothelial activation (endothelin, IL-6, IL-8, sE-selectin, soluble vascular adhesion molecule-1 [sVCAM-1], soluble intercellular adhesion molecule-1 [sICAM-1]) parameters were investigated 1, 3, 6, 9, 12, and 24 h after coronary reperfusion. Results 1) Parameters of myocardial injury (CK-MB, myoglobin) revealed increased levels at 1 h and 9 to 12 h after CABG. Levels at 12 h were lower in group B and D as compared to A and C. 2) Cytokines (IL-6, IL-8) showed increased levels 3 h after reperfusion with no difference between study groups. 3) Soluble adhesion molecules (E-selectin, VCAM-1, ICAM-1) were found increased in all groups 6 to 12 h after reperfusion. Lower levels were present in group D for E-selectin and VCAM-1. Conclusions The results indicate a sequence of cytokine and adhesion molecule release as a potential pathomechanism of myocardial reperfusion injury. Gradual decrease in the release of endothelial adhesion molecules in late myocardial injury was noted for blood cardioplegia and ischemic preconditioning. Amelioration of endothelial activation by means of preconditioning and blood cardioplegia may improve heart muscle recovery in open heart surgery with borderline ischemia time and organ dysfunction.      

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.     

Improved myocardial protection with blood and crystalloid cardioplegia

Although the results of coronary artery bypass surgery have been excellent, recent studies have demonstrated transient alterations in myocardial function and metabolism in spite of apparently adequate cardioplegic protection. Blood cardioplegia may provide better protection than crystalloid cardioplegia, but clinical studies remain inconclusive. Critical coronary stenoses limit cardioplegic delivery, and myocardial protection would be improved with either blood or crystalloid cardioplegia if the solution could be delivered beyond the coronary stenosis. The construction of proximal as well as distal anastomoses during a prolonged cross-clamp period permits more uniform cardioplegic delivery and immediate reperfusion when the cross clamp is released. This technique was used in a prospective randomized trial comparing blood and crystalloid cardioplegia. The long cross-clamp technique eliminated temperature gradients induced when cardioplegia was delivered into the aortic root. The technique of cardioplegic delivery may be as important as the solution used for cardioplegic protection. (J VASC SURG 1984;1:656-9.)     

缺血预处理对体外循环缺血心肌的保护效果

观察缺血预处理对体外循环(CPB)心脏高钾、冷停跳心肌的保护作用。方法:10只健康犬随机分为对照组(C组)与预缺血组(PC组),每组5只。CPB期间心脏高钾停跳,全心缺血60分.恢复灌注30分。PC组在CPB开始后、心脏停跳前增加预缺血5分钟、再灌注10分钟,对比观察阻断升主动脉前、后心肌超微结构、腺苷酸含量(ATP、ADP、AMP、TAN、EC)、脂质过氧化物丙二醛(MDA)以及血流动力学的变化。结果:(1)PC组在缺血30分钟、60分钟及开放升主动脉20分钟时,正常线粒体和糖原含量均接近缺血前水平,并明显高于C组(P<0.01);(2)心脏阻断前、后PC组心肌组织ATP、EC含量无显著变化,与C组同时比较差异十分显著(P<0.05或0.01);(3)缺血60分钟以及开放20分钟C组心肌MDA含量显著升高,与PC组比较差异十分显著(P<0.05或0.01);(4)开放升主动脉后,PC组血流动力学各项参数迅速恢复,其中CO、SV、CI、LVSW与C组比较差异有显著性(P<0.05或0.01)。结论:心肌缺血预处理明显增强体外循环心脏缺血再灌注期超微结构的保护效果。降低ATP的消耗,减少脂质过氧化物的形成,加速血流动力学的恢复。     

Intermittent antegrade warm myocardial protection compared to intermittent cold blood cardioplegia in elective coronary surgery--do we have to change?

OBJECTIVE: Intermittent antegrade warm blood cardioplegia (IAWBC) is a simple and cost-effective method of myocardial preservation. However, there are only few prospective trials comparing this type of cardioplegia to established cardioplegic strategies in elective on-pump coronary surgery with respect to myocardial protection and outcome. METHODS: In a prospective, randomized trial IAWBC (33 degrees C) (n=100) was compared to intermittent antegrade cold (4 degrees C) blood cardioplegia (n=100), regarding clinical outcome and myocardial protection using cardiac troponin-I (cTNI) and creatine kinase MB isoenzyme (CK-MB) measurements to assess ischemia. RESULTS: Preoperative parameters were comparable in both groups. Results demonstrated no differences in-between the groups regarding mortality (2.0% both), incidence of perioperative myocardial infarction (2 versus 3%), need for intra-aortic balloon pump (3 versus 4%), length of ICU stay (2.0+/-2.5 versus 2.1+/-3.0 days) and incidence of postoperative atrial fibrillation (41 versus 34%). However, the necessity of defibrillation after cardiac arrest (18 versus 43%, P<0.001) was significantly less frequent and of lower intensity (3.4+/-10.8 versus 10.8+/-20.6 J, P<0.001) in the IAWBC-group. Postoperatively the ischemia markers were significantly lower in the IAWBC-group, cTNI within the first 72 h (from P<0.001 to P=0.013) and even CK-MB within the first 24 h (from P=0.004 to P<0.011). CONCLUSION: IAWBC is a safe and simple method in elective on-pump coronary artery bypass surgery. Significantly lower ischemic markers suggest an improved myocardial protection compared to cold blood cardioplegia in these patients.     

Clinical appraisal of myocardial protection for coronary artery bypass grafting--efficacy of retrograde continuous cold blood cardioplegia]

Myocardial protection is one of the most important problems during coronary artery bypass grafting in patients with severe coronary artery disease. In this communication we have demonstrated retrograde continuous cold blood cardioplegia (RC-CBCP) in such cases with preferable results. In this study myocardial protection for CABG surgery was evaluated from the points of the myocardial distribution of cardioplegic solution, the changes of the value of myocardial enzyme, the recovery of cardiac function after unclamping of the aorta, and the results of operation [mortality and incidence of perioperative infarction (PMI)]. The effects of myocardial protections were compared among the following 4 groups: group-A (n = 38) where antegrade cardioplegia with 10 ml/min of CBCP was used; group-R (n = 52), retrograde cardioplegia with 10 ml/min of CBCP; group-Rm (n = 59), retrograde cardioplegia with 7-8 ml/100 g LVMW (left ventricular mass weight)/min of CBCP; group-Rmt (n = 65), RC-CBCP with terminal warm blood cardioplegia (TWB). Judging from myocardial temperature measured at the end of initial cardioplegic infusion, the myocardial distribution of cardioplegic solution in group-R was significantly favorable even in the distal area of severe coronary artery stenotic lesions exceeding 90% compared with group-A. The recovery of cardiac function assessed from the incidence of occurrence of spontaneous beating and the dose of cathecholamine at the weaning of cardiopulmonary bypass were most excellent in group-Rmt among the 4 groups. There was no significant difference in postoperative peak CK-MB and LDH-1 isoenzyme levels among the 4 groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ischemic preconditioning improves preservation with cold blood cardioplegia in valve replacement patients.

OBJECTIVE: The purpose of this study was to test the hypothesis that ischemic preconditioning improves myocardial protection in valve replacement patients undergoing cold-blood cardioplegic arrest and to study the mechanisms of human myocardial ischemic preconditioning initially. METHODS: Forty patients who required double valve replacement were studied. After the institution of cardiopulmonary bypass, 20 patients were preconditioned with two cycles of 3 min of aortic cross-clamping and 2 min of reperfusion before cardioplegic arrest (group IP). Twenty patients were not preconditioned as controls (group C). All hearts were arrested with 4 degrees C cold-blood cardioplegic solution. During perioperation, the blood samples were collected from coronary sinus and radial artery, which were used to measure calcitonin gene-related peptide (CGRP) and creatine kinase-MB (CK-MB). The right atrial myocardial tissue was collected to measure superoxide dismutase/malondialdehyde (T-SOD/MDA) and to observe myocardial ultrastructure. Hemodynamic date were measured. RESULTS: After reperfusion for 30 min, myocardial MDA was significantly lower in group IP than in group C (2.6+/-0.2 vs. 3.8+/-0.3 nM/mg) and T-SOD was significantly higher in group IP than in group C (13.1+/-12.1 vs. 9.2+/-1.2 IU/mg). Ischemic preconditioning significantly increased the production of myocardial CGRP just after preconditioning (92.0+/-4.1 vs. 52.3+/-4.5 pg/ml) and the begin of reperfusion (95.3+/-3.8 vs. 61.2+/-4.9 pg/ml), and deduced the release of CK-MB at 12 h post-reperfusion (77.5+/-9.2 vs. 136.5+/-8.9 IU/l). Preconditioning also improved cardiac function at 30 min and 12 h after reperfusion (cardiac index 2.8+/-0.3 vs. 2.3+/-0.2 l/min per m2 and 2.9+/-0.1 vs. 2.4+/-0.2 l/min per m2). CONCLUSIONS: Ischemic preconditioning enhance cardioplegic protection in valve replacement patients. The possible protective mechanism was that ischemic preconditioning decreased the production of oxygen free radicals.     

不同温度下含血停搏液对未成熟心肌的保护作用

目的 研究在不同温度下含血停搏液对未成熟心肌的保护作用,试图确定对未成熟心肌保护的最适宜温度范围,方法 使用离体心脏灌注模型,比较含血停搏液在１４、１７、２０、２４、２８℃时对未成熟兔（１４￣２１ｄ）心肌的保护效果。结果 各组温度对左室收缩压恢复率影响不大,但冠脉充量恢复纺、心肌含水量、心肌ＡＴＰ与Ｃａ＾２＋含蛭１７￣２０℃范围最优左室末压恢复率以１７℃最佳,恧主肌内丙二醛含量以２０℃最少。结论     

Intraoperative myocardial protection: a comparison of blood and asanguineous cardioplegia

Cardiac arrest was achieved in 84 patients using asanguineous cardioplegia and in 97 patients using cold blood potassium cardioplegia. The patient groups were similar in age, sex ratio, and preoperative risk factors. Other than the cardioplegic solution used, the conduct of each operation was identical. There were no differences in mean total pump time (118 minutes for the asanguineous cardioplegia group versus 117 minutes for the cold blood cardioplegia group) or cross-clamp time (73.5 versus 70 minutes, respectively). However, the blood cardioplegia group had a greater number of distal anastomoses per patient (3.9 versus 3.7; p less than 0.05). Myocardial protection was assessed clinically and by serial electrocardiograms. Cellular integrity was determined by release of the myocardial isoenzyme of serum creatine kinase (CK-MB). Cellular morphology was studied in 6 randomly selected patients in each group by electron microscopic examination of left ventricular myocardial samples obtained before and after bypass. Three patients given blood cardioplegia and 5 given asanguineous cardioplegia required intraaortic balloon counterpulsation at termination of bypass. There were no ultrastructural changes in either group. Electrocardiographic changes (Minnesota code) occurred in 12 of 84 patients receiving asanguineous cardioplegia versus 12 of 97 patients receiving cold blood potassium cardioplegia. To maintain a satisfactory cardiac index (greater than 2.0 L/min/m2), 38 of 84 patients given asanguineous cardioplegia versus 25 of 97 patients given blood cardioplegia required inotropic support up to 24 hours postoperatively (p less than 0.05). Infarct size determined from CK-MB release was significantly greater (p less than 0.05) in patients given asanguineous cardioplegia (36.27 gm-equivalents) than in those given blood cardioplegia (26.7 gm-equivalents).(ABSTRACT TRUNCATED AT 250 WORDS)