温、冷血停搏液间断灌注在瓣膜置换术中的心肌保护作用

目的比较体外循环下温血停搏液间断灌注与冷血停搏液间断灌注在瓣膜置换术中的心肌保护作用.方法36例心脏瓣膜置换术患者被随机分为温血间断灌注组(n=18)和冷血间断灌注组(n=18),分别于体外循环前,主动脉开放后30分钟、6小时、24小时采集动脉血,测血清心肌肌钙蛋白Ⅰ(cTnI)浓度.二尖瓣置换患者在主动脉开放时从冠状静脉窦抽取静脉血,检测乳酸浓度.部分患者于主动脉阻断前,开放后30分钟分别取右心房组织,透射电镜观察心肌超微结构.结果瓣膜置换术中温血停搏液间断灌注的心肌保护作用与冷血停搏液间断灌注近似,具有临床应用价值.两组各时间点血清cTnI浓度组间差异无显著性,温血间断灌注组冠状静脉窦血乳酸浓度高于冷血间断灌注组(P＜0.05),两组心肌超微结构变化近似.结论瓣膜置换术中温血停搏液间断灌注的心肌保护作用与冷血停搏液间断灌注近似,具有临床应用价值.     

心脏手术中温血心脏停搏液微流量连灌心肌保护效果的研究

为提高心脏手术中心保护的效果，将20例风湿性心瓣膜病手术患者随机分为温血组与冷血组。温血组术中采用温血心脏停搏液微流量连续灌注，冷血采用冷血心脏停搏液间断灌注行心肌保护。检测两组体外循环主动脉开放后即刻，主动脉开放后6、12、24、72小时血清心肌肌钙蛋白Ⅰ（cTnI）值；术中切取心房肌肉标本，电镜下观察超微结构变化，对比评价心肌保护效果。结果术前及主动脉开放即刻两组血清cTnI无显著性差异（P＞0．05）；主动脉开放后6、12、24、72小时温血组cTnI均显著低于冷血组，P＜0．01；超微结构检测示温血组心肌纤维及线粒体损伤显著轻于冷血组。认为温血心脏停搏液微流量连灌的心肌保护效果优于冷血心脏停搏液间断灌注。     

左旋卡尼汀心脏停搏液对主动脉开放后心脏复跳的临床研究

目的研究心脏手术病人术中应用左旋卡尼汀停搏液对主动脉开放后心脏复跳的影响。方法40倒心脏手术病人随机分为对照组和实验组，对照组术中应用St．ThomasⅡ号冷晶体心脏停搏液，实验组术中予St.ThomasⅡ号冷晶体心脏停搏液加入左旋卡尼汀6g／L。结果实验纽较对照组游离脂肪酸显著减少（P〈0．05），且主动脉开放后心脏复跳时间明显高于对照组（P〈0.05）；主动脉开放后发生心律失常及电除颤的例数明显低于对照组（P〈0．05）；实验组心脏自动复跳率明显高于对照组（P〈0．05）。结论左旋卡尼汀停搏液对缺血再灌注心肌有保护作用，其作用表现在多方面上，可以作为一类新型的抗心律失常药物和心肌保护药物应用于心内在视术中。     

HTK液在冠状动脉搭桥手术中的应用

目的 通过对比组氨酸-色氨酸-酮戊二酸(HTK)液及含血停搏液在体外循环下冠状动脉搭桥术(CABG)中的应用,探讨HTK液在CABG中的使用方法及其心肌保护效果.方法 将60例单纯行CABG的患者随机分为两组,HTK组术中使用HTK液正灌+逆灌的方法进行灌注停跳和心肌保护,对照组则使用常规的4∶1冷血高钾停搏液.在麻醉诱导后、升主动脉开放心脏复跳后10 min及术后6、12、24、48 h分别采血检测心肌肌钙蛋白T(cTnT)和肌酸激酶同工酶(CK-MB),并比较两组术后心脏自动复跳情况、后并行循环辅助时间、血管活性药物使用情况和术后心功能等指标.结果 HTK组心脏自动复跳率高于对照组、后并行循环辅助时间短于对照组(P均＜0.05);两组的cTnT和CK-MB浓度在升主动脉开放后均逐步升高,与升主动脉阻断前相比,P＜0.05,12 h达高峰,24 h后逐渐下降;HTK组cTnT和CK-MB的上升幅度在各时点均小于对照组(P均＜0.05).结论 在CABG手术中,HTK液正灌+逆灌的方法能够获得较好的心肌保护效果,其心肌保护效果优于冷血停搏液.     

前列地尔对体外循环术后的心肌保护作用

目的观察体外循环手术中晶体停搏液中加入前列地尔对心肌的保护作用。方法 40例行体外循环手术的患者,随机分为治疗组和对照组,每组各20例。治疗组术中冷晶体心肌停搏液中一次性加入前列地尔1 0μg,对照组则单纯应用冷晶体停搏液,两组其他条件相同,分别于麻醉后术前,体外循环转流30min,主动脉开放后,停机2h,停机6h,停机12h和停机24h共7个时间点取静脉血测量肌红蛋白（MYO）、肌酸激酶同工酶（CK-MB）和肌钙蛋白1（cTn1）的含量,记录升主动脉开放后心脏复跳及术后正性肌力药物的应用情况。结果 MYO从CPB 30min后开始升高,CPB 30min至术后24h治疗组明显低于对照组;CK-MB在主动脉开放后明显上升,复灌后治疗组明显低于对照组;cTn1从复灌后2h至24h治疗组低于对照组。心脏自动复跳率治疗组为85%,对照组为65%,两组比较无统计学意义。多巴胺用量治疗组明显低于对照组。结论在体外循环手术中,应用前列地尔作为心脏停搏液的组成成分,对心肌有较好的保护作用。     

左卡尼汀含血停搏液在心内直视术中的心肌保护作用

20例行心脏瓣膜置换手术患者随机分为对照组（冷血停搏液组）和实验组（冷血停搏液中加入左卡尼汀）各10例，分别于围术期多个时点取桡动脉血，测定血浆心型脂肪酸结合蛋白（HFABP）、肌钙蛋白（cTnI）、肌酸激酶同工酶（CK-MB）的水平，并观察手术前后心肌超微结构的变化。结果显示，两组术后HFABP、cTnI、CK-MB的水平均较术前显著升高，实验组上述指标均明显低于对照组。认为外源性左卡尼汀加入心脏停搏液能显著提高心肌保护效果。     

一体化综合性心肌保护对婴幼儿心肌超微结构的保护

目的：观察一体化综合性心肌保护方法对婴幼儿心肌超微结构的影响以评价其心肌保护效果。方法：30例复杂先天性心脏病患儿随机分成一体化综合性心肌保护组（综合组，含温血停搏液诱导停搏，冷血停搏液间歇灌注和终末温血灌注液复苏）、冷血停搏液间断灌注组（冷血组），及冷晶体停搏液间断灌注组（冷晶组），各10例。于心脏停跳即刻、缝合右心房切口前分别取小块右心房肌肉作光镜及电镜观察，并对线粒体、细胞核、肌纤维进行定量评估。结果：三组心肌均存在不同程度的损伤，冷晶组最重，综合组最轻。心肌超微结构评分在三组之间两两比较较有统计学意义（P〈0．01或P〈0．05）。结论：一体化综合性心肌保护作用优于冷血停搏液和冷晶体停搏液。     

还原型谷胱甘肽含血停搏液在心脏瓣膜置换术中的心肌保护作用

目的观察心脏含血停搏液加入还原型谷胱甘肽在心脏瓣膜置换术中的心肌保护作用.方法30例心脏瓣膜置换术患者随机分为两组,实验组(n=15)在心脏含血停搏液中加入还原型谷胱甘肽(剂量600 mg),对照组(n=15)单用心脏含血停搏液,分别经主动脉根部或切开主动脉经冠状动脉窦直接灌注,两组分别于麻醉诱导后、主动脉开放后2 h、6 h、24 h采集患者静脉血,测血清肌酸激酶MB同工酶(CK-MB)、乳酸脱氢酶(LDH)、心肌肌钙蛋白I(cTnI).结果两组主动脉开放后血清CK-MB、LDH、cTnI均较麻醉诱导后显著升高,实验组主动脉开放后的血清CK-MB、LDH、cTnI均较对照组显著降低(P均＜0.05-0.01),差异均具有统计学意义.结论还原型谷胱甘肽加入心脏停搏液中具有良好的心肌保护作用.     

尼可地尔超极化停搏对小香猪心肌的保护作用及其对c-Fos蛋白表达的影响

目的探讨尼可地尔超极化停搏对小香猪体外循环（CPB）下心肌的保护作用及其对c-Fos蛋白表达的影响。方法选择12只幼年小香猪,建立CPB模型。随机分为2组、每组6只,分别以高钾去极化含血停搏液（对照组）和尼可地尔超极化含血停搏液（实验组）经主动脉根部灌注使心脏停跳。记录心脏停跳前及复跳后心电活动情况;于CPB开始即刻（T1）,阻断升主动脉后45、90 min（T2、T3）,开放升主动脉45 min、90 min、6 h（T4、T5、T6）采静脉血检测心肌肌钙蛋白I（cTnI）水平;开放升主动脉90 min时留取心肌标本检测c-Fos蛋白及电镜超微结构变化。结果①心脏复跳后,实验组有4例出现一过性室颤,对照组仅有1例,两组一过性室颤发生率比较P〈0.05;②实验组T3、T4、T5时点血清cTnI浓度显著低于对照组（P〈0.05或〈0.01）;③实验组c-Fos蛋白阳性表达率为（0.18±0.09）%,对照组为（0.29±0.12）%,两组比较P〈0.05;④电镜下心肌超微结构显示实验组优于对照组。结论尼可地尔超极化停搏对CPB下心肌有明显保护作用,这可能与降低c-Fos蛋白表达有关。     

紫外线照射充氧自体血心脏停搏液对体外循环中心肌保护作用的研究

目的 研究紫外线照射充氧自体血（UBIO）心脏停搏液冠状动脉间断顺行灌注对体外循环（CPB）中心肌的保护作用。方法 将20只健康成年杂种犬（雌雄不拘）随机分为实验组和对照组，每组10只。CPB中实验组采用紫外线照射充氧自体血心脏停搏液问断灌注;对照组用等量4℃St．Thomas Ⅰ号冷晶体液作为心脏停搏液间断灌注，两组其余操作相同。结果 开放升主动脉后，实验组冠状静脉宴血清cTnI、CK-MB水平和左心室心肌MDA水平低于对照组（P〈0．05），左心室心肌SOD活性和ATP水平高于对照组（P〈0．05）;心脏自动复跳率明显高于对照组（P〈0．01）。心肌超微结构观察显示，实验组左心室心肌纤维结构完整，细胞内线粒体轻度水肿，而对照组心肌纤维部分断裂、溶解，线粒体基质外溢，糖原颗粒减少。结论 UBIO血心脏停搏液有较好的心肌保护作用，且能减少心脏停搏液的灌注次数，延长心脏停搏时间;本研究为UBIO血心脏停搏液的临床应用奠定了基础。     

Discontinuous warm cardioplegia in pediatric cardiac surgery: preliminary results

This article describes the use of warm cardioplegia in paediatric surgery. Warm blood enriched with potassium was injected every 15 minutes during aortic clamping in 770 operations. The efficacy and quality of this technique were assessed by the return of cardiac electrical activity, troponin I levels 12 hours after aortic clamping and the duration of postoperative ventilation in 3 groups of patients: ventricular septal defect under 6 months (N = 82), tetralogy of Fallot under one year (N = 55), simple transposition of the great arteries (N = 42). These results were compared retrospectively with those obtained using cold cardioplegia. The return of sinus rhythm was spontaneous in 99% of cases versus 77% with cold cardioplegia; the troponin I levels were under 10 ng/ml in 46% of cases versus 37% (NS). Patients operated for ventricular septal defect were ventilated 10 +/- 8 hours versus 13 +/- 10 hours with cold cardioplegia (p = 0.02). The children operated for tetralogy of Fallot were ventilated 8 +/- 4 hours versus 14 +/- 7 hours (p = 0.01) and those with simple transposition 56 +/- 71 hours versus 83 +/- 105 hours (NS). Warm cardioplegia, in the authors' experience, was associated with an improved postoperative course. In this group of 770 operations, 646 operated patients had a stay of less than two days in the intensive care unit.     

Transcardiac release of soluble adhesion molecules during coronary artery bypass grafting: effects of crystalloid and blood cardioplegia

BACKGROUND: Dysfunction of myocardium as a result of ischemia/reperfusion during coronary artery bypass grafting (CABG) is currently one of the biggest problems in cardiovascular surgery. In previous studies, it has been well established that activated leukocytes and coronary vascular endothelial cells play an important role in the development of cardiac tissue damage during ischemia followed by reperfusion. Interactions between both of these cell types require the expression of adhesion molecules on their surface. In certain conditions, on cell activation, the adhesion proteins may be released from activated cells in soluble form into circulation. The purpose of our study was to establish whether the use of blood cardioplegia modifies plasma levels of soluble intracellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin), and soluble L-selectin (sL-selectin) in comparison with crystalloid cardioplegia in patients undergoing CABG. METHODS: Patients undergoing CABG were classified into two groups to receive cold crystalloid cardioplegia (St. Thomas' Hospital) or cold blood cardioplegia (method of Buckberg), followed by a "warm-shot" of the solution. Coronary sinus and arterial blood samples were obtained from 50 patients (42 men and 8 women; age range, 34 to 73 years) before aortic cross-clamping, at the beginning of reperfusion, and after 30 min of reperfusion. Plasma levels of soluble adhesion molecules were measured using sensitive enzyme-linked immunosorbent assays. RESULTS: The transcardiac release of sICAM-1 and sVCAM-1 following myocardial ischemia/reperfusion during CABG was evident in both groups of patients. However, the increase of soluble forms of both of these adhesion proteins was more significant in the group of patients receiving crystalloid cardioplegia. Crystalloid cardioplegia resulted in decreased plasma level of sE-selectin in the coronary sinus blood sample after 30 min of reperfusion. No significant changes in plasma levels of sL-selectin in either group were observed. CONCLUSION: Cardioplegia may affect the release of soluble forms of adhesion molecules from ischemic myocardium and modify endothelium activation in patients undergoing CABG.     

Antegrade versus antegrade with retrograde delivery of cardioplegic solution in myocardial revascularisation. A clinical study in patients with triple vessel coronary artery disease

The effects of antegrade and antegrade with retrograde delivery of cardioplegic solution were evaluated in 60 patients who underwent myocardial revascularisation. All patients had triple vessel coronary artery disease and underwent revascularisation using arterial and vein grafts. Myocardial protection consisted of administration of the St.Thomas' Hospital cardioplegic solution, topical slushed ice and systemic hypothermia (28 degrees C-30 degrees C). The patients were categorised into: group A (n=30), who received antegrade cardioplegia alone, and group B (n=30), who received antegrade and retrograde cardioplegia. With the exception of the total dose of cardioplegic solution ('p'=0.02), there was no significant difference between the two groups. Cardiac function was assessed before and after the patient was weaned from the cardio-pulmonary bypass. There was a significant increase in the right atrial pressure and a significant decrease in the mean arterial pressure from the baseline ('p'<0.05), 10 minutes after cardiopulmonary bypass in group A. All patients in-group B had a spontaneous return to sinus rhythm after release of the aortic cross clamp, whereas 3 patients in group A required defibrillation to restore sinus rhythm. Intra aortic balloon pump support was necessary in 4 patients in group A, as against 1 patient in group B to terminate the cardiopulmonary bypass. The clinical outcome was similar in both groups. We conclude that the use of a combination of retrograde and antegrade cardioplegia facilitates early recovery of left ventricular function after coronary artery bypass grafting.     

Continuous tepid blood cardioplegia can preserve coronary endothelium and ameliorate the occurrence of cardiomyocyte apoptosis

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: These results point to an important explanation for the difference in cardiac recovery after hypothermic ischemia and arrest with various cardioplegic solutions.     

Reduction of oxidative stress does not affect recovery of myocardial function: warm continuous versus cold intermittent blood cardioplegia.

OBJECTIVE: To compare oxidative stress after cardiac surgery in patients treated with two different methods of myocardial protection: warm continuous versus cold intermittent blood cardioplegia. To correlate oxidative stress with postoperative myocardial dysfunction. DESIGN: Prospective, randomised, double blind, trial. SETTING: Institutional centre of cardiovascular surgery. PATIENTS: 20 patients were selected for coronary artery bypass surgery (CABG) on the following basis: stable angina, ejection fraction > 50%, double or triple vessel disease, no previous CABG or associated disease. Patients were randomised to two groups of 10 patients each. INTERVENTIONS: Patients underwent CABG with one of two different methods of myocardial protection and cardiopulmonary bypass. CBC group: intermittent cold blood antegrade-retrograde cardioplegia with moderate hypothermic cardiopulmonary bypass; WBC group: continuous warm blood antegrade-retrograde cardioplegia with mild hypothermic cardiopulmonary bypass. MAIN OUTCOME MEASURE: The index of oxidative stress used was the alteration of whole blood and plasma glutathione redox status. Samples were collected from the coronary sinus and peripheral vein before anaesthesia (T1), before aortic unclamping (T2), 15 minutes (T3), and 30 minutes (T4) after unclamping. Haemodynamic parameters were measured with thermodilution techniques. RESULTS: Oxidised glutathione and glutathione-cysteine mixed disulphide significantly increased in the coronary sinus plasma in the CBC group, and the overall redox balance of glutathione was decreased (P < 0.01) at T2-T4 versus T1, and compared with the WBC group. Comparable results were obtained for coronary sinus blood. There was no correlation between postoperative haemodynamic measurements and oxidative stress markers. CONCLUSIONS: Oxidative stress was significant in patients undergoing CABG using cold blood cardioplegia, while the warm technique minimised the effects of ischaemia. However, oxidative stress was not correlated with myocardial dysfunction following CABG.     

Prevention of myocardial intracellular edema induced by St. Thomas' Hospital cardioplegic solution.

During cardiac surgery, the heart is infused with cold crystalloid cardioplegic solutions such as St. Thomas' Hospital (StT) solution, which contains high concentrations of K+ and Mg2+. The high K+ and Mg2+ block impulse conduction and inhibit Ca2+ influx, thereby arresting the heart and reducing cardiac oxygen consumption. Nevertheless, myocardial edema and post-operative abnormalities have been noted after cardioplegia and attributed to ischemia and reflow or to hypothermia. We found, however, that cold StT (9 degrees C) was hypotonic and induced cell swelling in the absence of ischemic injury. Cell swelling in cold StT was not due to hypothermia alone, but rather was caused by KCl influx and was prevented by partially replacing Cl- with an impermeant anion. After exposure to cold StT, cells transiently shrank to less than control volume on rewarming in physiological saline (Tyrode's solution, 37 degrees C). The transient shrinkage was blocked by ouabain suggesting that Na+ loading of depolarized hypothermic cells and Na(+)-K+ pump activation on rewarming were responsible. Hypothermic ventricular cells seem to follow Donnan equilibrium, and the product of [K+] x [Cl-] in cardioplegic solutions affects cell volume in the absence of ischemic injury.     

Structural protection of the myocardial capillary endothelium by different forms of cardiac arrest and subsequent global ischemia at 5 degrees C.

BACKGROUND: In transplantation surgery sufficient myocardial protection achieved by cardioplegic cardiac arrest and deep hypothermia is a prerequisite for successful resumption of donor heart function. Intraischemic damage of the endothelium combined with capillary compression may lead to the "no-reflow phenomenon" during reperfusion, resulting in insufficient cardiac resuscibility. METHODS: We evaluated the endothelial ultrastructure after various common forms of cardiac arrest and subsequent ischemia in deep hypothermia. Canine hearts were arrested by aortic cross clamping and surface cooling with Tutofusin' (ACC) or by coronary perfusion with Custodiol (histidine tryptophane ketoglutarate, HTK solution), with University of Wisconsin solution (UW), or with St. Thomas' Hospital solution. After extirpation the hearts were incubated at 5 degrees C in the solution used for cardiac arrest. Myocardial samples were taken immediately after cardiac arrest and after 2h, 4h, 6h, and 10 h of global ischemia. The degree of structural damage was evaluated by a scoring system. Endothelial swelling was determined as the mean barrier thickness of the capillary endothelium. RESULTS: At all selected time points our results show that 1) after cardioplegia with St. Thomas' solution, the degree of endothelial cell swelling was higher than after aortic cross clamping; 2) using HTK or UW solution, the endothelial ultrastructure was better preserved than after aortic cross clamping or using St. Thomas' solution, whereby HTK was slightly better than UW; 3) using UW solution, endothelial cell swelling was a little (up to 10%) but significantly less than after HTK perfusion. CONCLUSIONS: With respect to the intraischemic structural preservation of endothelial cells, UW or HTK solution combined with deep hypothermia promises adequate protection, compared with other clinically used methods tested.     

A loss of taurine and other amino acids from ventricles of patients undergoing bypass surgery.

OBJECTIVE--To study the changes in amino acid content of left ventricles of patients during cardiac surgery that involves cardiopulmonary bypass and cold cardioplegia. DESIGN--Biopsy specimens (up to 10 mg wet weight) from the left ventricle of 30 patients undergoing coronary artery bypass graft and valve replacement surgery on cardiopulmonary bypass (protected by cold cardioplegia with St Thomas' solution) were taken immediately before the infusion of the cardioplegic solution and just before the removal of the cross clamp, and were analysed for their amino acid content. RESULTS--Of the most abundant cellular amino acids in the left ventricle taurine, glutamine, glutamate, and aspartate, but not alanine, showed a significant fall during the period of cross clamping. A rise in intracellular sodium (Na) is known to occur during cold cardioplegic arrest so that an activation of an amino acid/Na efflux, similar to that seen in animal experiments, seems a likely mechanism. The anomalous behaviour of alanine suggests some recovery of metabolism. CONCLUSIONS--The loss of alpha amino acids (by contrast with the loss of taurine) will depress protein synthesis and reduce energy reserves after cardiac surgery. Attempts to preserve the concentrations of intracellular alpha amino acids must be balanced against the need to regulate intracellular Na concentration and hence intracellular pH and calcium ions. The presence of alpha amino acids in the cardioplegic solution (or in a resuscitation solution) should maintain the intracellular concentrations and favour activation of the taurine/Na symport to oppose the rise in intracellular Na concentration. Because the reservoir of tissue taurine is limited, the potential benefits of increasing the concentration of taurine in the heart by diet before surgery and addition of alpha amino acids to the cardioplegic solution merits further assessment.     

Effects of different cardioplegic solutions on nitric oxide release from coronary vasculature in diabetic patients undergoing coronary artery bypass surgery.

OBJECTIVE: The aim of this study was to compare the effects of two different cardioplegic solutions on nitric oxide (NO) release from coronary vasculature in patients with type II diabetes mellitus undergoing coronary artery bypass grafting (CABG) surgery. METHODS: Forty patients undergoing elective CABG surgery were randomized to be given crystalloid (Group 1) or blood (Group 2) cardioplegia. Aortic and coronary sinus blood samples were taken at three different time periods and the release of NO from the coronary vasculature was determined by measuring its stable end-products, nitrite and nitrate. The difference between the aortic and coronary sinus concentrations of nitrite and nitrate represents the amount of NO released by coronary vascular bed. RESULTS: Before application of aortic cross-clamp, at T1 period, the levels of nitrite/nitrate from the coronary vasculature were similar in both groups (6.53+/-1.21 microM vs 6.07+/-1.24 microM , p>0.05). However after the removal of cross-clamp, a significant decrease in NO was observed in Group 1 as compared with Group 2 (4.21+/-0.73 microM vs 4.92+/-1.02 microM, p<0.01) . This decrease persisted at T3 period, after 30 minutes of reperfusion in group 1 being significantly different from group 2 (3.86+/-0.49 vs 4.37+/-0.72 microM, p<0.05). CONCLUSION: This study has shown that in patients with type II diabetes mellitus crystalloid cardioplegia causes a decrease in the release of NO from coronary vascular bed during aortic cross-clamp and reperfusion period whereas more physiologic blood cardioplegia did not. Our findings indicate that blood cardioplegia protects endothelial function better than crystalloid cardioplegia in diabetic patients.     

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 -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 -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.