Blood Cardioplegic Solution Research Articles

Pulmonary sequestration of cardioplegia administered via the aortic root during aortocoronary bypass surgery

A semi-quantitative method was devised of tracing blood flow through the heart and lungs at the time of cardioplegia delivery and circulatory arrest of the heart during coronary artery bypass graft surgery (CABG). There were no previous studies confirming or disputing an accepted 'observation' by cardiac surgeons that cardioplegia solution does enter the lung parenchyma during cardiopulmonary bypass (CPB). This study was conducted as part of a larger (n = 142) double-blind, randomised, controlled, clinical research study. The objective was initially to establish the efficacy of measures to prevent cardioplegia entering the lungs and, subsequently, to determine whether cardioplegia indeed circulates through the lung parenchyma or merely accumulates and 'pools'. A prospective study on 20 consecutive patients (5 per group) admitted for CABG was made. Technetium (Tc-99m), a radioactive isotope, was added to the cold blood cardioplegia solution prior to cardioplegia delivery in order to track flow of cardioplegia solution. An independent nuclear medicine radiographer measured the samples with the use of a 'Curimentor' dose calibrator for presence and quantity of radiation in the samples. Decay was factored into the results. The Tc-99m tracer samples were also analysed using Gamma Acquisition and Analysis on the Genie 2000vdm Well Counter to confirm the presence and quantity of Tc-99m. In the four groups, it was confirmed that the pulmonary artery (PA) vent is 90-100% effective in retrieving any cardioplegia solution not drained by the atriocaval cannulae. The PA vent is effective in preventing cold blood cardioplegia solution from entering the lungs. Any cardioplegia that does enter the lung parenchyma during CPB circulates through the lungs and can be retrieved by a vent in the left atrium. This method may be useful in other studies that require investigation.

Addition of the complement inhibitor dextran sulfate to blood cardioplegia solution attenuates myocardial reperfusion injury associated with extracorporeal circulation in a porcine model of cardiopulmonary bypass

Addition of the complement inhibitor dextran sulfate to blood cardioplegia solution attenuates myocardial reperfusion injury associated with extracorporeal circulation in a porcine model of cardiopulmonary bypass

Resuscitation of Non-Beating Donor Hearts Using Continuous Myocardial Perfusion: The Importance of Controlled Initial Reperfusion

Warm ischemia is a major cause of cardiac allograft failure in transplants from non-heart-beating donors. To minimize myocardial ischemia, we used a continuous myocardial perfusion technique for resuscitation of donor hearts. The purpose of the present study was to investigate an optimal duration of controlled initial reperfusion. Cardiac arrest was induced by asphyxia in 18 donor pigs. The hearts were harvested 30 minutes after global warm ischemia. Continuous myocardial reperfusion was immediately commenced from the aortic root with blood cardioplegic solution (20 degrees C, 40 mm Hg) and then with oxygenated blood (20 degrees to 37 degrees C, 40 to 60 mm Hg). Animals were divided into three groups according to the duration of the initial reperfusion: group I = 5 minutes, group II = 20 minutes, and group III = 60 minutes. Orthotopic transplantation was performed while keeping the heart beating by continuous myocardial perfusion. Cardiac function was evaluated before anoxia and after transplantation. Lactate extractions were determined during reperfusion. Myocardial edema was assessed by heart weight and posterior wall thickness of the left ventricle. Recovery rates of cardiac function in group II hearts after transplantation were better than in groups I and III (cardiac output, 61% +/- 9% versus 41% +/- 5% versus 44% +/- 4%, respectively; p < 0.05; left ventricular end-systolic pressure-volume ratio, 64% +/- 8% versus 36% +/- 9% versus 42% +/- 6%, respectively; p < 0.05). Lactate extractions in groups II and III returned to 0 within 20 minutes of reperfusion. Myocardial edema after transplantation in group II hearts was less than in groups I and III. The best recovery was observed in the non-beating donor hearts resuscitated by continuous myocardial perfusion when the initial controlled reperfusion with lukewarm blood cardioplegic solution at 40 mm Hg lasted for 20 minutes.

Repair of symptomatic neoaortic aneurysm after third-stage palliation for hypoplastic left heart syndrome

Repair of symptomatic neoaortic aneurysm after third-stage palliation for hypoplastic left heart syndrome

Myocardial Protective Effect of Histidine-Tryptophan-Ketoglutarate Solution and Cold Blood Cardioplegic Solution in Pediatric Cardiac Surgery

Background: There is limited data on comparisons between the effect of histidin-etryptophan-ketoglutarate (HTK) solution and cold blood cardioplegic (CBC) solution in pediatric cardiac surgery. The purpose of this study was to compare the myocardial protective effect of HTK solution and CBC solution in patients undergoing pediatric cardiac surgery. Materials and Methods: We selected 49 patients with ventricular septal defect and atrial septal defect. HTK solution was used in 21 patients and CBC solution was used in 28 patents. HTK solution was given as a single dose, whereas CBC solution was used in the usual multi-dose method. The incidence of EKG change and concentration of Troponin T and CK-MB were compared for the evaluation of myocardial damage. Results: There were no significant differences in the incidence of ST, T segment change by EKG and serial cardiac enzyme levels between two groups. Conclusion: These results suggested that the myocardial protective effect of HTK solution was similar to CBC solution in simple pediatric cardiac surgery.

Protective Effects of L-arginine Blood Cardioplegia on Immature Myocardium

目的 探讨左旋精氨酸加入Thomas Ⅱ停搏液对未成熟心肌的保护效果.方法 2～3周龄新西兰大白兔20只,随机分为2组,每组10只.建立Langendoff离体心脏灌注模型.对照组:Thoma s Ⅱ号停搏液灌注加低温;实验组:左旋精氨酸加入Thomas Ⅱ号停搏液灌注并行低温.全心平均停循环90min,再灌注30min.观察指标:冠脉流量恢复率(CFR)、心肌丙二醛(MDA)/超氧化物岐化酶(SOD)含量、心肌三磷酸腺苷(ATP)含量、心肌磷酸肌酸激酶(CK)漏出量和乳酸脱氢酶(LDH)漏出量.结果再灌注末实验组心肌MDA含量低于对照组,而SOD含量高于对照组;实验组CFA和再灌注末心肌ATP含量高于对照组;实验组心肌含水量、CK和LDH漏出量低于对照组.结论左旋精氨酸加入含血Thomas Ⅱ号停搏液中可改善未成熟心肌的保护作用。

Effects of Crystalloid, Blood and Celsior Solutions on Porcine Coronary Endothelial Function After Heart Transplantation

Coronary endothelial dysfunction occurs early after heart transplantation and predicts the development of cardiac allograft vasculopathy. Cardioplegic solutions may cause endothelial injury. The present study aimed to assess the effects of cardioplegic solutions (crystalloid, blood and Celsior) used at the time of graft harvesting on endothelial function and intimal hyperplasia 1 month after heart transplantation. A porcine heterotopic heart transplantation model was used. Three experimental groups were studied: crystalloid, blood and Celsior solutions were used for induction of cardiac arrest. Epicardial coronary arteries of native and allograft hearts were studied 1 month after transplantation in organ chambers. Endothelium-dependent relaxations to serotonin, bradykinin and calcium ionophore were assessed. Coronary neointimal proliferation was evaluated using histomorphometric studies. Endothelium-dependent relaxations to serotonin and to calcium ionophore were significantly decreased in all 3 experimental groups vs controls (p<0.05). Endothelium-dependent relaxations to bradykinin were significantly reduced in the crystalloid group compared with the Celsior and blood groups and controls (p<0.05). There was a significantly lower rate of severe intimal hyperplasia in the Celsior group compared to the crystalloid and blood groups (p<0.05). Celsior cardioplegic solution represents the solution of choice in terms of preservation of endothelial function and lower incidence of severe coronary intimal hyperplasia following transplantation compared with crystalloid and blood cardioplegia solutions. These early results could translate into a reduction of the long-term incidence of cardiac allograft vasculopathy and improve graft survival.

Pyruvate-fortified cardioplegia suppresses oxidative stress and enhances phosphorylation potential of arrested myocardium

Cardioplegic arrest for bypass surgery imposes global ischemia on the myocardium, which generates oxyradicals and depletes myocardial high-energy phosphates. The glycolytic metabolite pyruvate, but not its reduced congener lactate, increases phosphorylation potential and detoxifies oxyradicals in ischemic and postischemic myocardium. This study tested the hypothesis that pyruvate mitigates oxidative stress and preserves the energy state in cardioplegically arrested myocardium. In situ swine hearts were arrested for 60 min with a 4:1 mixture of blood and crystalloid cardioplegia solution containing 188 mM glucose alone (control) or with additional 23.8 mM lactate or 23.8 mM pyruvate and then reperfused for 3 min with cardioplegia-free blood. Glutathione (GSH), glutathione disulfide (GSSG), and energy metabolites [phosphocreatine (PCr), creatine (Cr), P(i)] were measured in myocardium, which was snap frozen at 45 min arrest and 3 min reperfusion to determine antioxidant GSH redox state (GSH/GSSG) and PCr phosphorylation potential {[PCr]/([Cr][P(i)])}. Coronary sinus 8-isoprostane indexed oxidative stress. Pyruvate cardioplegia lowered 8-isoprostane release approximately 40% during arrest versus control and lactate cardioplegia. Lactate and pyruvate cardioplegia dampened (P < 0.05 vs. control) the surge of 8-isoprostane release following reperfusion. Pyruvate doubled GSH/GSSG versus lactate cardioplegia during arrest, but GSH/GSSG fell in all three groups after reperfusion. Myocardial [PCr]/([Cr][P(i)]) was maintained in all three groups during arrest. Pyruvate cardioplegia doubled [PCr]/([Cr][P(i)]) versus control and lactate cardioplegia after reperfusion. Pyruvate cardioplegia mitigates oxidative stress during cardioplegic arrest and enhances myocardial energy state on reperfusion.

Dysphagia: An unusual presentation of giant aneurysm of the right coronary artery and supravalvular aortic stenosis in Williams syndrome

Clinical Summary A 56-year-old patient with dysphagia was admitted to our hospital for evaluation. On medical history, he was found to have neurodevelopmental delay and was receiving antihypertensive therapy. An extrinsic stenosis on the midportion of the esophagus did not allow us to complete full gastroenteral screening. Computed tomographic scanning showed the presence of a mediastinal mass 11 cm in diameter compressing the esophagus (Figure 1), which was diagnosed as an isolated aneurysm of the right sinus of Valsalva. The echocardiogram showed the presence of an SVAS with a gradient of 70 mm Hg, and the pulmonary trunk and bifurcation were normal. Angiography showed normal peripheral pulmonary vascularization and normal left coronary artery anatomy. The right coronary artery at its origin from the aorta opened up in a huge dilatation of 11 cm. The patient was taken to the operating theater on an urgent basis. Cardiopulmonary bypass was instituted through femorofemoral cannulation. The heart was emptied, and the chest was opened. At opening, it was possible to visualize a huge aneurysmal mass compressing the right atrium and superior vena cava and covering the ascending aorta (Figure 2, A). The aorta was crossclamped and transected. Warm blood cardioplegic solution was administered directly into the coronary ostia. When the aorta

Pediatric myocardial protection: a cardioplegic strategy is the “solution”

This article describes the experimental infrastructure and subsequent successful clinical application of a comprehensive cardioplegic strategy that limits intraoperative injury and improves postoperative outcomes in pediatric patients. The infant heart is at high risk of damage from poor protection as a result of preoperative hypertrophy, cyanosis, and ischemia. These factors may also make the immature (pediatric) heart more sensitive to cardioplegic arrest compared with the mature (adult) heart. The preoperative factors of cyanosis and pressure volume overload are discussed, followed by the infrastructure of the strategies of warm induction and reperfusion with substrate enhancements, multidose cardioplegia, and a “modified” integrated approach to allow ischemia only when visualization is needed in pediatric surgeries. The importance of using a blood cardioplegia solution, with reduced calcium, increased magnesium, and low perfusion pressure are also shown. A practical clinical framework based on these experimentally proven principles is then presented to allow the surgeon to apply these strategies clinically. The results of using these principles are depicted in a series of 567 patients, including 93 patients with hypoplastic left heart syndrome. Applications of these concepts should improve the safety of protection of the infant heart and reduce postoperative morbidity and mortality.

Myocardial protection in adult cardiac surgery: current options and future challenges.

Current techniques of myocardial protection are evolving with the use of less conventional modalities of cardioplegia and have reduced the morbidity and mortality of cardiac operations. Blood cardioplegic solutions appear superior to cold cardioplegia in terms of myocardial protection and adjuncts as glutamate/aspartate enhancement, antioxidant supplementation, nitric oxide donors and maintenance of calcium homeostasis seem effective. In the near future, further experimental and clinical investigations about pharmacological preconditioning, sodium-hydrogen exchangers inhibition and gene therapy need to be addressed to well define their potential role in the improvement of current techniques of myocardial protection that are suboptimal in high-risk clinical settings.

Pyruvate-enhanced cardioprotection during surgery with cardiopulmonary bypass

Objectives To determine whether pyruvate-fortified cardioplegia solution provides cardioprotection superior to lactate-based cardioplegia solutions in patients undergoing elective coronary revascularization, with specific attention to post-surgical recovery of left ventricular performance as well as biochemical markers of ischemic injury. Design Prospective, randomized, semi-blinded human trial. Setting Community-based academic medical center. Participants Thirty adult patients undergoing elective coronary artery bypass graft surgery. Interventions Patients were randomized to two 4:1 blood cardioplegia solutions, one pyruvate enhanced and the other lactate based. Hemodynamic and laboratory variables were measured in all patients at pre-cross-clamp, post-cross-clamp, and 4, 6, 8, and 12 hours after bypass. Measurements and main results Relative to lactate-based cardioplegia, pyruvate-fortified cardioplegia sharply increased left ventricular stroke work at 4 to 12 hours after bypass ( p < 0.001), lowered coronary sinus troponin I and creatine phosphokinase-MB activities 67% ( p < 0.001) and 53% ( p < 0.01), respectively, and increased coronary sinus hemoglobin O 2 saturation 18% ( p < 0.001). Ten patients treated with lactate cardioplegia required β-adrenergic inotropic support postbypass, but only 4 pyruvate-treated patients required β-adrenergic support ( p = 0.067). Pyruvate cardioplegia shortened postsurgery hospitalization from 6.3 ± 0.3 to 5.2 ± 0.1 days ( p < 0.002). Conclusions Pyruvate-fortified cardioplegia mitigated myocardial injury during coronary artery bypass surgery and facilitated postsurgical recovery of cardiac performance. Thus, pyruvate-enhanced cardioplegia may provide cardioprotection superior to lactate-based solutions during surgical cardiac arrest.

Leukocyte-depleted terminal blood cardioplegia provides superior myocardial protective effects in association with myocardium-derived nitric oxide and peroxynitrite production for patients undergoing prolonged aortic crossclamping for more than 120 minutes

Objectives This study was designed to examine the myocardial protective effect of leukocyte-depleted terminal blood cardioplegia in association with nitric oxide and peroxynitrite production, especially for patients undergoing prolonged aortic crossclamping. Methods Fifty-four patients (34 men, 20 women, mean age 56.7 ± 12.7 years) undergoing aortic valve replacement were randomly allocated to one of two groups; group LDTC (n = 27) received 10 minutes of leukocyte-depleted terminal blood cardioplegic solution, and group CONT (n = 27) served as controls. Each group was subdivided into 2 groups: aortic crossclamping for less than 120 minutes in groups LDTC-S (n = 13) and CONT-S (n = 14); aortic crossclamping for 120 minutes or more in groups LDTC-L (n = 14) and CONT-L (n = 13). Results After aortic unclamping, group LDTC-L showed higher incidence of spontaneous defibrillation (78.6% vs 30.8%, P = .0213), higher plasma nitrate + nitrite in the coronary sinus effluent (32.5 ± 4.1 vs 28.7 ± 3.0 μmol/L, P = .0013), lower differences between coronary sinus effluent and arterial blood in the percentage ratio of nitrotyrosine to tyrosine (myocardium-derived peroxynitrite; 2.987% ± 0.576% vs 3.951% ± 0.952%, P = .0036), and plasma polymorphonuclear-elastase (113.9 ± 21.3 vs 155.5 ± 41.6 μg/L, P = .0029) and malondialdehyde (2.75 ± 0.67 vs 4.02 ± 0.96 μmol/L, P = .0005) than group CONT did. Postoperatively, group LDTC-L showed lower human-heart fatty acid–binding protein (111.4 ± 25.2 vs 156.4 ± 38.6 IU/L, P = .0013), lower creatine kinase–muscle and brain (19.2 ± 4.7 vs 24.8 ± 6.5 IU/L, P = .0120), and smaller requirement of catecholamine (5.44 ± 2.29 vs 8.45 ± 3.42 μg · kg −1 · min −1, P = .0122). There were no significant differences in these parameters between groups LDTC-S and CONT-S. Conclusions This study demonstrated that leukocyte-depleted terminal blood cardioplegia provided superior myocardial protective effects and regulated myocardial-derived nitric oxide and peroxynitrite production only for patients undergoing aortic crossclamping for more than 120 minutes. The results suggest that prolonged aortic crossclamping deteriorates the tolerance to leukocyte-mediated myocardial injury accompanied by endothelial dysfunction associated with nitric oxide and peroxynitrite production.

A new role for cardioplegic buffering: should acidosis or calcium accumulation be counteracted to salvage jeopardized hearts?

Objectives: Thirty minutes of unprotected ischemia produced a jeopardized heart that was treated with a blood cardioplegic solution containing the natural erythrocyte and protein buffers. Cardioplegic pH was changed to 7.7 (buffered) or 7.2 (nonbuffered), and this was tested alone and after pretreatment with Na +-H + exchange blockade (cariporide) to define their protective effects. Methods Twenty-four Yorkshire-Duroc pigs (27-34.5 kg) underwent 30 minutes of normothermic global ischemia, followed by 30 minutes of aortic clamping during protection with buffered (n = 12) or nonbuffered (n = 12) glutamate-aspartate–enriched blood cardioplegic solution. Twelve hearts (6 buffered and 6 nonbuffered) were pretreated with intravenous cariporide (5 mg/kg) 15 minutes before ischemia. Results Severe and comparable left ventricle dysfunction followed buffered or nonbuffered cardioplegia: Preload recruitable stroke work recovered to 56% ± 21% and 45% ± 20% of baseline levels; creatine kinase MB, conjugated dienes, and myeloperoxidase activity markedly increased; moderate myocardial edema occurred; and endothelin-1 increased 2-fold more than baseline values. Cariporide pretreatment caused a similar return of preload recruitable stroke work to 86% ± 9% and 90% ± 6% after buffered or nonbuffered cardioplegia ( P < .05 vs nonpretreated groups), allowed only minor creatine kinase MB and conjugated diene changes, and reduced endothelin-1 release 3-fold compared with hearts without sodium-hydrogen exchange blockage. Conclusions The severe ischemia-reperfusion injury of 30 minutes of normothermic ischemia is not altered by an acidic or alkalotic pH cardioplegic solution. Correction of damage is achieved by adding Na +-H + exchange blocker therapy before treatment with buffered and nonbuffered solutions; thus, sodium-hydrogen exchange inhibition plays a more vital role in recovery than pH management.

The behavior of Troponin I and CKMB mass in children who underwent surgical correction of congenital heart malformations

OBJECTIVE: To analyze the behavior of troponin (TROP I) and CKMB mass (CKMBm) in regards to the addition of magnesium in cardioplegic solutions; and also the influence of per-operative factors. METHOD: A total of 28 children with ages ranging from 3 to 108 months were studied. The mean weight was 11.8 kg. Eighteen were male. The patients were divided into two groups. Sixteen children in group I (GI) and 12 in group II (GII). The patients in GI received cold blood cardioplegic solution with magnesium (12 mEq/L) and potassium chloride (20 mEq/L) at 20 mL/kg. The patients in GII received the same solution without magnesium. Six blood samples were collected for serum analysis of the concentration of TROP I and CKMBm. The blood samples were collected before clamping the aorta and at 1, 6, 24, 48 and 72 hours after aorta clamping termination. RESULTS: There were no statistical differences in the TROP I and CKMBm levels between the two groups. Among the per-operative factors cyanosis influenced the TROP I and CKMBm levels. Additionally, the aorta clamping time influenced the TROP I levels. CONCLUSIONS: The addition of magnesium in the cardioplegic solution was not associated with different levels of TROP I and CKMBm. Cyanosis and aorta clamping time interfered with peak TROP I levels.

Bovine valved xenograft conduits in the extracardiac Fontan procedure

Total cavopulmonary connection has been proposed as a rational alternative to atriopulmonary connection for complex Fontan operations. de Leval and colleagues proposed the concept of direct cavopulmonary connection as a way to minimize kinetic energy loss in the Fontan circuit. Total cavopulmonary anastomosis with the extracardiac conduit technique has gained favor because it streamlines the venous flow pattern and reduces the incidence of atrial arrhythmias. There are a number of potential advantages of the extracardiac conduit approach over other modifications of the Fontan procedure, including the improved hydrodynamics in the cavopulmonary connection. Conduits of different material have been used for the extracardiac Fontan procedure, examples of these conduits are the Dacron tube, the polytetrafluoroethylene tube (Gore-Tex; W. L. Gore & Associates, Inc, Flagstaff, Ariz), the homograft, and the pericardial tube, and each one has advantages and disadvantages. Bovine jugular vein xenograft (Medtronic’s Contegra, Medtronic, Inc, Minneapolis, Minn) has been used successfully to reconstruct the right ventricular outflow tract in patients with congenital heart disease, with promising early results. The Contegra conduit is a biologic valved conduit consisting of a glutaraldehyde-preserved heterologous bovine jugular vein with a trileaflet venous valve. The advantages of using the Contegra xenograft are easy availability, different size options, and the presence of a valve in the conduit. In this report we present potential advantages of using a xenograft valved conduit to construct the extracardiac Fontan connection between the inferior vena cava (IVC) and the pulmonary artery (PA).

Continuous Tepid Blood Cardioplegia Can Preserve Coronary Endothelium and Ameliorate the Occurrence of Cardiomyocyte Apoptosis

In modern cardiac surgery, crystalloid or blood cardioplegic solutions have been used widely for myocardial protection; however, ischemia does occur during protection with intermittent infusion of cold crystalloid or blood cardioplegic solutions. The present study was designed to evaluate the effect of different cardioplegic methods on myocardial apoptosis and coronary endothelial injury after global ischemia, cardiopulmonary bypass (CPB), and reperfusion in anesthetized open-chest dogs. The dogs were classified into five groups to identify the injury of myocardium and coronary endothelium: group 1, normothermic CPB without cardiac arrest; group 2, hypothermic CPB with continuous tepid blood cardioplegia, and with cardiac arrest; group 3, hypothermic CPB with intermittent cold blood cardioplegia, and with cardiac arrest; group 4, hypothermic CPB with intermittent cold crystalloid cardioplegia, and with cardiac arrest; and group 5, sham-operated control group. During CPB, cardiac arrest was achieved with different cardioplegia solutions for 60 min, followed by reperfusion for 4 h before the myocardium and coronary arteries were harvested. Coronary arteries were harvested immediately and analyzed by scanning electron microscopy. Cardiomyocytic apoptosis was detected using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling, Western blot, and DNA ladder methods. Regardless of the detection method used, significantly higher percentages of apoptotic cardiomyocytes were found in group 3 and group 4 than in other groups. Expression of caspase-3 correlated with increased apoptosis. Scanning electron microscopy revealed severe endothelial injury of coronary arteries in group 3 and group 4. These results point to an important explanation for the difference in cardiac recovery after hypothermic ischemia and arrest with various cardioplegic solutions.

Blood cardioplegic protection in profoundly damaged hearts: role of Na +-H + exchange inhibition during pretreatment or during controlled reperfusion supplementation

Background Inhibition of the Na +/H + exchanger before ischemia protects against ischemia-reperfusion injury, but use as pretreatment before blood cardioplegic protection or as a supplement to controlled blood cardioplegic reperfusion was not previously tested in jeopardized hearts. Methods Control studies tested the safety of glutamate-aspartate–enriched blood cardioplegic solution in 4 Yorkshire-Duroc pigs undergoing 30 minutes of aortic clamping without prior unprotected ischemia. Twenty-four pigs underwent 30 minutes of unprotected normothermic global ischemia to create a jeopardized heart. Six of these hearts received normal blood reperfusion, and the other 18 jeopardized hearts underwent 30 more minutes of aortic clamping with cardioplegic protection. In 12 of these, the Na +/H + exchanger inhibitor cariporide was used as intravenous pretreatment (n = 6) or added to the cardioplegic reperfusate (n = 6). Results Complete functional, biochemical, and endothelial recovery occurred after 30 minutes of blood cardioplegic arrest without preceding unprotected ischemia. Thirty minutes of normothermic ischemia and normal blood reperfusion produced 33% mortality and severe left ventricular dysfunction in survivors (preload recruitable stroke work, 23% ± 6% of baseline levels), with raised creatine kinase MB, conjugated dienes, endothelin-1, myeloperoxidase activity, and extensive myocardial edema. Blood cardioplegia was functionally protective, despite adding 30 more minutes of ischemia; there was no mortality, and left ventricular function improved (preload recruitable stroke work, 58% ± 21%, p < 0.05 versus normal blood reperfusion), but adverse biochemical and endothelial variables did not change. In contrast, Na +/H + exchanger inhibition as either pretreatment or added during cardioplegic reperfusion improved myocardial recovery (preload recruitable stroke work, 88% ± 9% and 80% ± 7%, respectively, p < 0.05 versus without cariporide) and comparably restored injury variables. Conclusions Na +/H + exchanger blockage as either pretreatment or during blood cardioplegic reperfusion comparably delays functional, biochemical, and endothelial injury in jeopardized hearts.

Comparison between warm blood and crystalloid cardioplegia during open heart surgery

Objective: This study was designed to compare the degree of myocardial protection afforded by warm blood and cold crystalloid cardioplegia in a group of patients undergoing elective coronary artery bypass surgery. Methods: Seventeen patients, were randomly assigned to Group A ( n=9), who received crystalloid cardioplegic solution, and Group B who received warm blood cardioplegic solution ( n=8). Before the aorta was clamped, and 10 min after reperfusion, blood samples from the coronary sinus were obtained to assay α-tocopherol, β-carotene, ubiquinol, and thiobarbituric acid reactive substances (TBARS). At the same intervals, biopsies from the left ventricle were obtained to determine ultrastructural alterations. Results: No significant changes were observed between preischemia and reperfusion values for both blood and crystalloid groups concerning α-tocopherol, β-carotene, and ubiquinol, and no differences between groups were detected. Values for TBARS in group A were 3.49±0.3 and 5.27±0.45 μM for presichemia and reperfusion samples, respectively ( P<0.01). In group B values were 2.6±0.3 and 3.54±0.3 μM, respectively ( P=NS). For electron microscopy studies, semiquantitative analysis showed a significant mitochondrial damage in reperfusion biopsies from group A (grades 0, 3 and 4). In group B, no significant changes were observed in mitochondrial damage between preischemia and repefusion biopsies (except for grade 0). Conclusion: These results indicate that blood cardioplegia affords better protection to the myocyte than crystalloid cardioplegia.

Effects of Albumin Supplementation during Cardioplegia Administration: An In Vitro Analysis

Increasing, the colloid osmotic pressure (COP) of blood cardioplegia (BCP) may reduce myocardial edema and preserve cardiac function following cardiopulmonary bypass (CPB). The purpose of this study was to quantify the effects of albumin (ALB) supplementation on cardioplegia COP through an in vitro analysis. A self-contained cardioplegia delivery system administered supplemental ALB to four BCP ratios (1:1, 4:1, 8:1, and 20:1). In Group A, 25% ALB was combined with BCP at four delivery rates (0,13, 25, and 50 mL ALB/L BCP), with a delivery rate of 0 mL ALB/L BCP serving as the control for all groups. Twenty-five percent ALB was added to crystalloid to create carrier solutions containing 12.5, 25, or 50 g ALB/L in Group B, while Group C combined an ALB delivery rate of 50 mL ALB/L BCP with each of the three carrier solutions. Endpoints included initial and post-supplementation hematocrit, total serum protein (TSP), and COP. Without supplemental ALB, TSP was less affected with increasing blood to crystalloid ratios (1:1-81.7 ± 6.2%, 4:1-40.6 ± 5.1%, 8:1-20.6 ± 4.1%, 20:1-6.0 ± 5.7%). The TSP of 1:1 and 4:1 BCP increased (p &lt; .0003 and p &lt; .02) across all methods of supplementation, while 8:1 BCP was similarly increased (p &lt; .008), except with 12.5 and 25 g ALB/L carrier solutions. The greatest change from baseline COP was seen with the lower blood to crystalloid ratios (1:1-64.3 ± 5.0% and 4:1-39.5 ± 10.5%). In higher ratios, the effects of dilution were less profound (14.6 ± 4.2 ± 4.2% and 20:1-6.0 ± 1.9%). COP of 1:1 BCP increased (p &lt; .008) whenever ALB was added. In conclusion, TSP and COP of blood cardioplegic solutions is increased by supplemental albumin administration with quantitative enhancement dependent upon the dilutional effects of the blood to crystalloid ratio.