超极化停搏对体外循环中心肌细胞膜微粘度变化的影响

目的比较超极化停搏和去极化停搏对体外循环(CPB)中心肌细胞膜流动性变化的影响,评价超极化停搏液的心肌保护作用. 方法根据随机数字表法将72只家猫均分为3组,每组24只.对照组:不阻断上、下腔静脉和主动脉,仅行并行循环180分钟;去极化停搏组:阻断主动脉60分钟,再灌注90分钟,心脏停搏液使用St.Thomas液(K 16mmol/L);超极化停搏组:心脏停搏液使用含吡那地尔的St.Thomas液(K 5mmol/L),其余处理与去极化停搏组相同.应用荧光偏振法测定心肌细胞膜的微粘度(η),以η的倒数表示心肌细胞膜流动性. 结果去极化停搏组主动脉阻断期间心肌细胞膜η值明显上升,且于再灌注期间进一步升高;超极化停搏组主动脉阻断期间亦呈升高趋势,但各时间点η值均明显低于去极化停搏组(P＜0.01). 结论超极化停搏比去极化停搏能更有效地维持CPB中缺血-再灌注心肌细胞膜的流动性,从而起到更好的心肌保护作用.     

Cold blood as the vehicle for potassium cardioplegia

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.     

Ischemia-tolerance following cardioplegic arrest in human patients and in experimental animals.

Cardiac biopsies were taken from the hearts of 40 patients undergoing open heart surgery for acquired and congenital disease. Tissue samples were taken prior to aortic cross-clamping, at the end of the ischemic period, and 20 minutes after reperfusion. Cardiac arrest was induced with Kirsch's cardioplegic solution at mild hypothermia (28-30 degrees C). Electron-microscopy of these tissue samples showed that cardioplegic arrest allows safe recovery with a tolerable degree of cellular alterations following ischemic periods of approximately 45 minutes. This period of reversible ischemia agreed well with similar studies in dogs that were completed by metabolic studies. ATP4-time in these dogs was 60 minutes under conditions closely resembling those at operationmin spite of the similarity between ischemia tolerance times, marked discrepancies existed on the ultrastructural level. Human hearts showed, generally, a much more marked degree of cellular alterations. The good correlation between ultrastructural alterations and the metabolic status of the canine heart can, therefore, not be used to predict levels of metabolites from human electron-micrographies.     

Ultrastructural and cytochemical correlates of myocardial protection by cardiac hypothermia in man

We report observations on ultrastructural and cytochemical changes in the myocardium after hypothermic protection in 21 patients who underwent cardiac operation. Two general categories of hypothermic protection were studied. (1) topical cooling during anoxic arrest and moderate general hypothermia (10 patients with aortic valve replacement, Group 1) and (2) intermittent perfusion during moderate general hypothermia combined with topical cooling (11 patients with multiple valve replacement, Group II). Transmural left ventricular biopsies were taken at the start of the cardiopulmonary bypass and shortly after the end of aortic cross-clamping. In Group I (cross-clamp time, 51 +/- 12 minutes) only minor pathologic changes of the myocardial fine structure were found, with no differences among the left ventricular layers. In most mitochondria, structure remained intact but the mitochondrial granules disappeared. Cytochrome-c-oxidase activity was unchanged. In Group II (total cross-clamp time, 83 +/- 16 minutes) the subendocardium was well preserved. Slight subcellular damage comparable with that of resulting from topical cooling was seen in all hearts even after a total cross-clamp period of 106 minutes. Cytochrome-c-oxidase activity was unchanged. In the subepicardium, however, a positive correlation was found between the severity of ultrastructural damage and total cross-clamp time (p less than 0.05). Matrix clearing, damage to the cristae and the mitochondrial membranes, and nuclear abnormalities occurred when the aorta was cross-clamped for morethan 60 minutes. Cytochrome-c-oxidase activities decreased in these samples. It is concluded that: (1) no significant subcellular injury was found in hearts cooled topically during 1 hour of anoxic arrest; and (2) in hearts protected by intermittent perfusion during moderate general hypothermia and additional external cooling, the subendocardium was well preserved for anoxic periods of up to 106 minutes. However, after 60 minutes of aortic cross-clamping subcellular damage increased progressively in the subepicardium.     

Topical Cardiac Cooling by Recirculation: Comparison of a Closed System Using a Cooling Pad with an Open System Using a Topical Spray

Topical cardiac cooling plays an important part in maintaining myocardial hypothermia during cardiac operations under hypothermic cardioplegic arrest. We have compared two systems of topical cooling in which the cooling fluid is recirculated. In one system the cold fluid circulates through a sealed plastic cooling pad wrapped around the heart; in the other it is sprayed over the surface of the heart.In dogs undergoing 60 minutes of hypothermic cardioplegic arrest, the cooling pad was ineffective: it did not adequately cool the anterior left ventricular wall or the interventricular septum. Under the same conditions, the spray system produced myocardial temperatures 6° to 12°C lower than the cooling pad system. In limited clinical tests, the cooling pad was unable to sustain overall myocardial hypothermia and there was difficulty in maintaining contact between the heart and the pad during coronary operations. Since the topical spray can maintain profound global myocardial hypothermia regardless of the position of the heart, we conclude that it is superior to the cooling pad system.     

Improved myocardial recovery after cardioplegic arrest with an oxygenated crystalloid solution

Possible enhancement of myocardial protection by oxygenation of a crystalloid cardioplegic solution was evaluated in a three-part study. In Part I, canine hearts underwent ischemia followed by heterogeneous cardioplegic arrest for 45 to 60 minutes. Oxygenation led to improved recovery in the left anterior descending region (47% versus 86% recovery, p less than 0.05) (15 minutes of ischemia) and in the circumflex region (9.5% versus 52% recovery, p less than 0.05) (30 minutes of ischemia). Part II was a blind prospective randomized study in 12 patients. It examined creatine kinase, myoglobin, and lactate as well as coronary sinus flow, oxygen consumption, and cardiac work 1 hour after aortic cross-clamping during atrial and during ventricular pacing. No significant difference was demonstrable between control and oxygenated solutions. In Part III, 57 coronary bypass patients were protected with a nonoxygenated solution while 94 patients received an identical oxygenated solution. Twelve-hour creatine kinase levels were similar in the nonoxygenated (9.5 +/- 16 IU, +/- standard deviation) and oxygenated (11 +/- 22 IU) groups if the cross-clamp interval was 28 minutes or less. In patients subjected to longer than 28 minutes of arrest, the 12 hour creatine kinase MB levels were more than twice as high in the nonoxygenated group (26.5 +/- 26 IU) compared to the oxygenated group (9.9 +/- 14 IU, p less than 0.05). In this canine model of heterogeneous cardioplegia and in the routine conduct of coronary bypass operations, oxygenated crystalloid cardioplegia is superior to an identical nonoxygenated solution.     

钾通道开放剂心脏超极化停搏保护效果的研究

目的 对比观察大量三磷酸腺苷（ＡＴＰ）敏感性钾通道开放剂吡那地尔对常温／低温体外循环（ＣＰＢ）心脏超极化停跳缺血心肌的保护作用。方法 １８只犬随机分３组,每组６只,低温超极化组（ＬＨ）：阻断升主动脉后,心脏灌注４℃含吡那地尔停跳液,ＣＰＢ血温为２６～２８℃,开放前复温至３７℃,全心缺血６０ｍｉｎ,恢复灌注３０ｍｉｎ;常温超极化组（ＷＨ）：ＣＰＢ血温３５～３７℃,心脏灌注３７地７０含吡那地尔（５０μｍｏｌ／Ｌ）停跳液,余同ＬＨ组;对照组（Ｃ）;无吡那地尔的标准Ｓｔ、Ｔｈｏｍａｓ停跳液,余３７℃含昆那地尔（５０ｕｍｏｌ／Ｌ）停跳液,余同ＬＨ组;对照组（Ｃ）：无吡那地尔的标准Ｓｔ．Ｔｈｏｍａｓ停跳液,余同ＬＨ组,对比观察吡那地尔心脏超极化停跳不同时相各项指标的变化。结果 （１）停复跳情况：ＬＨ组、Ｃ组灌注后心脏停跳较     

Effects of coenzyme Q10 added to a potassium cardioplegic solution for myocardial protection during ischemic cardiac arrest

To evaluate effects of coenzyme Q10 added to a potassium cardioplegic solution for myocardial protection, 17 mongrel dogs underwent 60 minutes of ischemic cardiac arrest under cardiopulmonary bypass. Cardiac arrest was induced by infusing the cardioplegic solution into the aortic root every 20 minutes. Experimental animals were divided into three groups according to the cardioplegic solution used. In Group 1, we used our clinical potassium cardioplegic solution (K+, 22.31 mEq/L); in Group 2, potassium cardioplegic solution with coenzyme Q10 added (coenzyme Q10, 30 mg/500 ml of solution); and in Group 3, cardioplegic solution with coenzyme Q10 solvent. Exogenous coenzyme Q10 in the cardioplegic solution provided significantly high myocardial stores of adenosine triphosphate and creatine phosphate and a low level of lactate during induced ischemia and reperfusion. Furthermore, percent recovery of the aortic flow in Group 2 was significantly higher than that in the other two groups. Ultrastructures of the ischemic myocardium in Group 2 were better preserved than those in Group 1. Addition of coenzyme Q10 to potassium cardioplegia resulted in improved myocardial oxygen utilization and accelerated recovery of myocardial energy metabolism after reestablishment of circulation.     

Does Local Cardiac Hypothermia During Cardiopulmonary Bypass Protect the Myocardium from Long-Term Morphological and Functional Injury?

Twenty-eight dogs were subjected to 90 minutes of hypothermic (30°C) cardiopulmonary bypass with moderate hemodilution. In 6 dogs the heart was vented and beating for 60 minutes. Eight dogs underwent ventricular fibrillation with coronary perfusion (VF + CP). In 14 dogs the aorta was cross-clamped for 60 minutes while the myocardium was protected by local cardiac hypothermia (ICA + LCH). Eighteeen animals survived. Hemodynamic studies at seven weeks revealed no major differences among the three groups. At postmortem examination, no gross scarring was noted in any heart. Microscopical examination of 14 hearts was completely normal. In the VF + CP group, 2 hearts had isolated microscopical scars. Similar linear subendocardial scars (<1.5 × 0.5 mm) were noted in 2 hearts subjected to ICA + LCH. Survival after 60 minutes of VF + CP or ICA + LCH did not result in long-term morphological injury to or functional impairment of the myocardium.     

Long-term morphologic and hemodynamic evaluation of the left ventricle after cardiopulmonary bypass. A comparison of normothermic anoxic arrest, coronary artery perfusion, and profound topical cardiac hypothermia.

In order to assess the long-term effects of cardiopulmonary bypass (CPB) in combination with pupular methods of myocardial protection, 37 dogs were placed on CPB for 100 minutes with the use of a bubble oxygenator without hemodilution. A separate group (I) of eight normal dogs served as a control for assessment of hemodynamic changes. The operative groups were as follows: II, continuous coronary perfusion with an empty, beating heart for 60 minutes at 35 degrees C.; III, hypothermic anoxic arrest (aortic occlusion) for 60 minutes with topical cold saline lavage (4 degrees C.); IV, anoxic arrest for 60 minutes at 35 degrees C. Subgroups of Groups III and IV received intracoronary perfusion with Ringer's lactate or Sacks' solution during aortic occlusion and were compared with those animals receiving no perfusion. Survival in Groups II and III was significantly better than in Group IV (82 and 92 per cent vs. 45 per cent). Coronary perfusion with Ringer's lactate or Sack's solution did not influence survival. The 23 survivors from all groups underwent left heart catheterization and LV cineangiography 5 months after operation. All three operative groups had significant elevation of LVEDP and depression of maximum developed dp/dt when compared with normal dogs. Ejection fraction was significantly depressed in Groups III and IV, and there was evidence of left ventricular hypokinesia and/or akinesia in all three operative groups. Differences in function between Groups II, III, and IV were not significant. The use of intracoronary solutions during anoxic arrest did not significantly influence these functional alterations. Evidence of subendocardial fibrosis was found in each of the operative groups, with the most marked changes found in the normothermic arrest group. Moderate fibrosis was present, however, in some survivors in both the continuous coronary perfusion and topical hypothermic arrest groups. These data indicate that although survival is greatly enhanced when coronary artery perfusion or topical hypothermia is used, neither method prevents chronic deterioration in ventricular function nor the development of subendocardial fibrosis.     

Pretreatment with lidoflazine, a calcium-channel blocker. Useful adjunct to heterogeneous cold potassium cardioplegia

Ten mongrel dogs were studied to determine if pretreatment with lidoflazine would protect the canine myocardium during aortic cross-clamping when circumflex coronary artery occlusion limits the distribution of cold potassium cardioplegia. A canine right heart bypass preparation was used. Regional function was determined with a sonomicrometer. Twenty minutes before aortic cross-clamping, lidoflazine or solvent was administered in a random, blind fashion. A circumflex artery snare prevented the cardioplegic solution from entering the circumflex artery. A 100 minute arrest period with cardioplegic infusion every 20 minutes was followed by 45 minutes of reperfusion before global and regional function were reevaluated. In the group receiving solvent, postarrest function in the circumflex region recovered to only 30% of prearrest values (p less than 0.05), a marked functional deterioration. In the group protected by lidoflazine, function in the circumflex region returned to 90% of prearrest values (NS). Function in the left anterior descending (LAD) regions of both groups demonstrated full recovery after arrest. Global left ventricular function was well preserved in both groups and failed to reflect the damaged, malfunctioning region in the group receiving solvent. These findings suggest that pretreatment with lidoflazine can improve myocardial protection when delivery of cardioplegia is not homogeneous.     

Enhanced myocardial preservation by nicotinic acid, an antilipolytic compound. Improved cardiac performance after hypothermic cardioplegic arrest

The effect of nicotinic acid, an antilipolytic drug, on myocardial preservation was studied on the basis of cardiac performance after 2 hours of cardioplegic arrest. Isolated in situ pig hearts were subjected to 120 minutes of hypothermic potassium (35 mEq) crystalloid cardioplegic arrest followed by 60 minutes of reperfusion. The experimental group received nicotinic acid 0.08 mmol/L 15 minutes before cardioplegic arrest, whereas the control group received 15 minutes of unmodified perfusion. There was a marked decline in myocardial creatine phosphate levels during cardioplegic arrest in both groups that returned to the baseline level during reperfusion without a significant intergroup difference, and adenosine triphosphate levels remained stable throughout the experiment in both groups. Myocardial oxygen consumption during reperfusion was significantly higher in hearts treated with nicotinic acid, which was consistent with a significantly greater cardiac contractile force as evaluated by isovolumetric left ventricular pressure measurements. There appeared to be less cardiac membrane damage as measured by creatine kinase release during reperfusion, which was significantly inhibited by treatment with nicotinic acid. The present study supports the conclusion that nicotinic acid improves cardiac performance after hypothermic cardioplegic arrest.     

Warm heart surgery: experience with long cross-clamp times

Although hypothermic cardioplegic arrest prolongs the period of ischemic arrest by reducing oxygen demands, it leaves the heart dependent solely on anaerobic metabolism for its energy demands and exposes it to the detrimental effects of hypothermia. Consequently, myocardial protection is compromised, and safe aortic occlusion time is limited to 120 minutes. As electromechanical arrest accounts for 90% of myocardial oxygen consumption, we hypothesized that an ideal state of the heart might be chemically arrested and perfused with warm blood, ie, aerobic arrest. We applied this approach to myocardial protection in 308 consecutive procedures. To assess the adequacy of this method, we reviewed the results in a group of 22 patients in whom the aortic cross-clamp time was, of necessity, greater than or equal to 3 hours (mean time, 204 minutes; range, 180 to 393 minutes). Nineteen of the patients represented a high operative risk with grade 3 or 4 left ventricular function and New York Heart Association class III or IV. All hearts resumed spontaneous normal sinus rhythm without defibrillation, and 21 patients were easily weaned from bypass within minutes of removal of the aortic cross-clamp without inotropic or intraaortic balloon pump support. Mortality was 4.5%, low-output syndrome occurred in 4.5%, and there were no perioperative myocardial infarctions. Our results suggest that warm aerobic arrest is safe and effective in prolonged high-risk procedures, virtually eliminating the period of ischemia, limiting the period and injury of reperfusion, and abolishing the detrimental effects of hypothermia.     

Effects of Conventional Hypothermic Ischemic Arrest and Pharmacological Arrest on Myocardial Supply/Demand Balance During Aortic Cross-Clamping

Aortic cross-clamping may produce ischemic damage due to a discrepancy between supply and demand. Supply is determined by noncoronary collateral flow and substrate stores, and demand by electromechanical activity, wall tension, and temperature. The effects of 60 minutes of conventional hypothermic ischemic arrest were compared to those of pharmacological arrest.Noncoronary collateral blood supply was comparable in both groups during cross-clamping. With ischemic arrest, mechanical activity and endocardial electrical activity persisted and wall tension fell progressively. With pharmacological arrest, electromechanical activity stopped in less than 1 minute but returned (with increased wall tension) nearly 1 hour. Thirty minutes following reperfusion, coronary flow was redistributed away from subendocardium after ischemic arrest and toward endocardium after pharmacological arrest. Myocardial performance was depressed severely after conventional arrest and only mildly after pharmacological arrest.We conclude that aortic cross-clamping is safer with pharmacological arrest than with ischemic arrest. The cardioplegic solution modifies the supply/demand balance favorably, but it is washed out by noncoronary collateral blood supply.     

Verapamil and myocardial preservation in patients undergoing coronary artery bypass surgery

The value of verapamil hydrochloride as a myocardial preservative when administered prior to or during periods of myocardial ischemia was studied in patients with normal preoperative cardiac function during elective coronary artery bypass grafting. Myocardial protection included systemic hypothermia (28 degrees C) and hypothermic hyperkalemic cardioplegia. Patients were randomly divided into four groups. Group 1 received intravenous administration of verapamil prior to aortic cross-clamping. Group 2 received intravenous verapamil plus verapamil in the cardioplegic solution. Group 3 received verapamil in the cardioplegic solution only. Group 4 was given no verapamil. Oxygen extraction during the reperfusion period was greatest in Group 4. However, the incidence of pacing was 50 to 78% in Groups 2 and 3, who were given verapamil in the cardioplegic solution. These groups also had a greater need for inotropic agents for discontinuation of cardiopulmonary bypass (CPB). This study indicates that verapamil may be a useful pretreatment prior to CPB and ischemia, but is not effective and may even be detrimental when administered during ischemic periods to patients with good myocardial function.     

Comparison of three cardioplegic solutions during hypothermic ischemic arrest in neonatal blood-perfused rabbit hearts

Inadequate myocardial preservation continues to be an important cause of postoperative morbidity and mortality after pediatric cardiac operations. To investigate methods of improving preservation in neonatal myocardium, we compared three cardioplegic solutions with topical hypothermia during 120 minutes of ischemic arrest in isolated, blood-perfused, neonatal rabbit hearts. Topical hypothermia (15 degrees C) without cardioplegia resulted in 71% +/- 5% recovery of preischemic contractile function. A high potassium (30 mEq/L) cardioplegic solution resulted in a 76% +/- 6% recovery of function, not significantly different from that obtained with hypothermia alone. In contrast, the St. Thomas' Hospital and H?pital Lariboisiere cardioplegic solutions resulted in recoveries of 89% +/- 6% and 88% +/- 7%, respectively, both of which were significantly greater (p less than 0.001) than recoveries obtained with the high potassium solution or hypothermia alone. Thus the cardioplegic solutions used at St. Thomas' Hospital and H?pital Lariboisiere provided excellent protection during 2 hours of hypothermic ischemic arrest in neonatal rabbit hearts and resulted in functional recovery superior to that achieved with hypothermia alone or with the high potassium cardioplegic solution.     

Etiology of atrioventricular-conduction abnormalities following cardiac surgery

Atrioventricular-nodal-conduction abnormalities following cardiac surgery have been attributed to the potassium ion in cardioplegic solutions. To clarify the etiology of these rhythm problems, 15 dogs were subjected to (I) 60 min 4°C potassium cardioplegic arrest; (II) 30 min normothermic ischemic arrest; or (III) cardiac hypothermia without ischemia. In sinus rhythm and during atrial pacing, A-H and H-V intervals, Wenckebach cycle length (WCL), atrial- and AV-nodal refractory periods (ARP and NRP) were measured at 37°C before and 30 min after arrest (groups I and II) and at various myocardial temperatures (group III). Following cardioplegic arrest and reperfusion, all AV-nodal-conduction properties were unchanged from preischemic values. In contrast, unprotected ischemia significantly prolonged AV-nodal-conduction time (P < 0.01) and myocardial hypothermia resulted in prolonged WCL (P < 0.01), prolonged functional NRP (P < 0.05), in addition to delayed A-H interval (P < 0.05). The data suggest that properties of AV-nodal conduction are preserved following potassium cardioplegic arrest, but impaired by ischemic injury or persistent local cardiac hypothermia.     

Hemodynamic effects of mexiletine and disopyramide after cardioplegic arrest

To study the hemodynamic side effects of mexiletine and disopyramide when administered before cardioplegic arrest 15 dogs underwent sham cardiac surgery with a 90-min period of aortic cross-clamping. 5 dogs served as control, 5 were given 8 mg/kg/day mexiletine and another five 11 mg/kg/day disopyramide for 1 week before surgery. On the day of surgery a continuous infusion was started. After reperfusion treated animals exceeded their preischemic blood pressure and regained their preoperative cardiac output. Compared to control animals left ventricular work was higher in the treated animals after reperfusion. The two tested type I antiarrhythmics tend to add to myocardial protection when given before cardioplegic arrest and do not exhibit negative inotropic side effects.     

Is Reperfusion Injury from Multiple Aortic Cross-Clamping a Current Myth of Cardiac Surgery?

Four hundred eighty adult patients undergoing cardiac operations had systemic and topical hypothermic anoxic arrest supplemented with potassium chloride pharmacological cardioplegia in a prospective randomized study. Group 1 (217 patients) had continuous aortic cross-clamping and one single anoxic arrest period during the cardiac portion of the operation which resulted in a transmural myocardial infarction rate of 8.3%, myocardial “injury” incidence of 12.4%, 4.6% cardiac-related deaths, 11.5% and 24.8% severe and malignant ventricular arrhythmias, 21.7% rate of severe vasopressor usage, a mean group serum glutamic oxaloacetic transaminase (SGOT) of 140 ± 39 IU, and a mean group lactic dehydrogenase (LDH) of 636 ± 78.2 IU. Group 2 (263 patients) had intermittent aortic cross-clamping with multiple reperfusion intervals, which resulted in a significantly lower incidence of transmural myocardial infarction at 1.9% (p < 0.01), rate of myocardial injury at 5.66% (p < 0.02), number of cardiac deaths at 0.76% (p < 0.02), 8.7% and 16.0% severe and malignant ventricular arrhythmias (p < 0.01), severe vasopressor utilization rate of 14.3% (p < 0.05), mean group SGOT at 72.0 ± 3.1 IU (p < 0.01), and mean group LDH at 471.0 ± 12.3 IU (p < 0.05) than Group 1. These results do not support the contention that intermittent aortic cross-clamping in conjunction with hypothermia and pharmacological cardioplegia leads to increased clinical cardiac damage compared with continuous aortic cross-clamping. The converse is implied, in that the anoxic heart may benefit from the physiological effects of briefly reperfused oxygenated blood.     

Effect of multidose cardioplegia and cardioplegic solution buffering on myocardial tissue acidosis

Multidose administration of cardioplegic solution during cardiac operation is intended to maintain both electromechanical arrest of the heart and myocardial hypothermia as well as to remove accumulated metabolites of anaerobic glycolysis. This study was conducted to assess the effect of multidose infusion of three different types of cardioplegic solution on tissue acidosis during global myocardial ischemia. Three groups of five dogs each were placed on cardiopulmonary bypass and the aorta was cross-clamped for 3 hours. The hearts were maintained at a constant temperature (20 degrees C) and cardioplegic solution was infused at an initial dose of 500 ml and five supplementary doses of 250 ml administered every 30 minutes. Group 1 received a crystalloid solution weakly buffered with sodium bicarbonate, Group 2 received a blood-based solution, and Group 3 received a crystalloid solution strongly buffered with histidine (Bretschneider's solution). The buffering capacities of the solutions used in Groups 2 and 3 were 40 and 60 times, respectively, that of the solution used in Group 1. The average myocardial tissue pH at the end of 3 hours of ischemia was 6.54 +/- 0.07 in Group 1, 7.23 +/- 0.05 in Group 2, and 7.19 +/- 0.06 in Group 3 (Group 1 significantly lower than Groups 2 and 3). Multidose infusion of a cardioplegic solution with low buffering capacity was unable to prevent the progressive development of tissue acidosis during 3 hours of ischemia. However, the multidose infusion of either blood-based or crystalloid solutions with high buffering capacity completely prevented any further reduction of tissue pH after the first 30 minutes of ischemia.