Ventricular fibrillation seen just after declamping of the aorta is an undesirable condition causing myocardial injury. To return to normal rhythm, often internal shocks are applied. But defibrillation itself can also...Ventricular fibrillation seen just after declamping of the aorta is an undesirable condition causing myocardial injury. To return to normal rhythm, often internal shocks are applied. But defibrillation itself can also contribute to myocardial injury. So prevention of fibrillation is more important than treatment. 236 patients undergoing coronary artery by-pass surgery were included in this retrospective clinical study. 144 of those patients were operated using modified St. Thomas’ Hospital cardioplegic solution, for stopping the heart. In the other 92 patients, plegisol cardioplegic solution was used. We compared the two groups for the development of ventricular fibrilation after declamping of the aorta. In the modified St. Thomas’ Hospital group, ventricular fibrillation after declamping of the aorta was seen less frequently, this being statistically significant (22.2% vs. 52.2%, p = 0.026). This study shows that the modified St.Thomas’ Hospital cardioplegic solution is preferred for avoiding ventricular fibrillation occuring just after declamping of the aorta.展开更多
To evaluate the effects of warm blood cardioplegic solution on myocardial protection, normothermic induction and terminal perfusion of oxygenated blood cardioplegia in combination with intermittent administration of c...To evaluate the effects of warm blood cardioplegic solution on myocardial protection, normothermic induction and terminal perfusion of oxygenated blood cardioplegia in combination with intermittent administration of cold blood cardioplegia during ischemia were studied in an isolated working rat heart model.The experimental protocol consisted of a 120 min cardioplegic arrest followed by 45 min normothermic reperfusion. Myocardial content of adenosine triphosphate (ATP), recovery of the left ventricular function, release of creatine phosphokinase (CPK) and ultrastructure of myocardium were assessed before and after ischemia. The results showed that the hearts preserved with warm blood cardioplegic induction and terminal perfusion had significantly higher levels of ATP,better recovery of cardiac function and lower releases of CPK than those receiving cold blood cardioplegia alone, with myocardial tissue being of generally normal structure. These findings suggest that warm induction and terminal perfusion of blood cardioplegic solution can accelerate myocardial metabolic and functional recovery, preserve high-energy phosphate, reduce myocardial injury and enhance myocardial protection.展开更多
Direct effects of a high-dose aprotinin on the normally perfused hearts and the myocardial protection after ischemia and reperfusion were investigated in an isolated working rat heart model. In trial I, hearts had no ...Direct effects of a high-dose aprotinin on the normally perfused hearts and the myocardial protection after ischemia and reperfusion were investigated in an isolated working rat heart model. In trial I, hearts had no ischemia and were perfused with either K-H solution or the K-H solution containing aprotinin (200KIU/ml) for 55 min. No statistically significant difference was observed in hemodynamics betweem the two groups. In trial Ⅱ, hearts were exposed to 150 minperiod of global ischemia at 15℃ with 4℃ multidose St. Thomas'Ⅱ solution (STS). The control group I received norma1 K-H solution; the group Ⅱ was treated with the solution with aprotinin added. The group, was similar to the group Ⅰ and received the STS enriched with aprotinin. On reperfusion, the recovery of hearts in group, was significantly better than those of the group Ⅰand Ⅱ, as reflected by better hemodynamics and myocardial oxygen consumption,lower level myocardial enzymes, higher myocardial ATP levels and milder myocardial ultrastructural injury. There was no difference between the group Ⅰand Ⅱ. These results suggest that the aprotinin at a dose of 200 KIU/ml has no harmful effects on normally perfused hearts and has a marked myocardial protective effect on the prolonged myocardial ischemia when used in cold crystalloid cardioplegia.展开更多
Background Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels （KATe） ...Background Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels （KATe） were the end effectors of cardio-protection. But whether mitochondrial KATe plays an important role in hyperpolarizing cardioplegia is not apparent. The present study investigated the effect of hyperpolarizing cardioplegia containing pinacidil （a nonselective KATe opener） on ischemia/repeffusion injury in rat hearts, especially the role of mitochondrial KATe in pinacidil hyperpolarizing cardioplegia. Methods Sprague-Dawley rat hearts were Langendorff-perfused for 20 minutes with Krebs-Henseleit buffer at 37℃ before equilibration. Cardiac arrest was then induced in different treatments： there was no arrest and ischemia in the normal group, the control group were arrested by clamping the aorta, depolarizing caidioplegia （St. Thomas solution containing 16 mmol/L KCI） and hyperpolarizing cardioplegia groups used St. Thomas solution containing 0.05 mmol/L pinacidil and 5 mmol/L KCI to induce cardiac arrest in group hyperkalemic and group pinacidil, in group hyperkalemic ＋ 5-hydroxydecanote （5HD） and Pinacidil ＋ 5HD, 5HD （0.1 retool/L） was added to the above two solutions to block mitochondria KATe channels. Global ischemia was then administrated for 40 minutes at 37℃, followed by 30 minutes of reperfusion. At the end of equilibration and reperfusion, hemodynamics, ultrastructure, and mitochondrial function were measured. Results In the control group, ischemia/reperfusion decreased the left ventricular developed pressure, heart rate, coronary flow, mitochondrial membrane potential, impaired mitochondrial respiratory function, increased reactive oxygen species and left ventricular end diastolic pressure. Damage to myocardial ultrastructure was also evident. Both depolarized arrest and especially hyperpolarized cardioplegia significantly reduced these lesions. 5HD partially blocked the beneficial effects of pinacidil cardioplegia but showing no effects on hyperkalemic arrest. Conclusions Pinacidil cardioplegia provides better cardioprotection with preservation of hemodynamics, ultrastructure, and mitochondrial function than traditional cardioplegia. The mitochondria KATe channels may play an important role in the protection mechanism.展开更多
文摘Ventricular fibrillation seen just after declamping of the aorta is an undesirable condition causing myocardial injury. To return to normal rhythm, often internal shocks are applied. But defibrillation itself can also contribute to myocardial injury. So prevention of fibrillation is more important than treatment. 236 patients undergoing coronary artery by-pass surgery were included in this retrospective clinical study. 144 of those patients were operated using modified St. Thomas’ Hospital cardioplegic solution, for stopping the heart. In the other 92 patients, plegisol cardioplegic solution was used. We compared the two groups for the development of ventricular fibrilation after declamping of the aorta. In the modified St. Thomas’ Hospital group, ventricular fibrillation after declamping of the aorta was seen less frequently, this being statistically significant (22.2% vs. 52.2%, p = 0.026). This study shows that the modified St.Thomas’ Hospital cardioplegic solution is preferred for avoiding ventricular fibrillation occuring just after declamping of the aorta.
文摘To evaluate the effects of warm blood cardioplegic solution on myocardial protection, normothermic induction and terminal perfusion of oxygenated blood cardioplegia in combination with intermittent administration of cold blood cardioplegia during ischemia were studied in an isolated working rat heart model.The experimental protocol consisted of a 120 min cardioplegic arrest followed by 45 min normothermic reperfusion. Myocardial content of adenosine triphosphate (ATP), recovery of the left ventricular function, release of creatine phosphokinase (CPK) and ultrastructure of myocardium were assessed before and after ischemia. The results showed that the hearts preserved with warm blood cardioplegic induction and terminal perfusion had significantly higher levels of ATP,better recovery of cardiac function and lower releases of CPK than those receiving cold blood cardioplegia alone, with myocardial tissue being of generally normal structure. These findings suggest that warm induction and terminal perfusion of blood cardioplegic solution can accelerate myocardial metabolic and functional recovery, preserve high-energy phosphate, reduce myocardial injury and enhance myocardial protection.
文摘Direct effects of a high-dose aprotinin on the normally perfused hearts and the myocardial protection after ischemia and reperfusion were investigated in an isolated working rat heart model. In trial I, hearts had no ischemia and were perfused with either K-H solution or the K-H solution containing aprotinin (200KIU/ml) for 55 min. No statistically significant difference was observed in hemodynamics betweem the two groups. In trial Ⅱ, hearts were exposed to 150 minperiod of global ischemia at 15℃ with 4℃ multidose St. Thomas'Ⅱ solution (STS). The control group I received norma1 K-H solution; the group Ⅱ was treated with the solution with aprotinin added. The group, was similar to the group Ⅰ and received the STS enriched with aprotinin. On reperfusion, the recovery of hearts in group, was significantly better than those of the group Ⅰand Ⅱ, as reflected by better hemodynamics and myocardial oxygen consumption,lower level myocardial enzymes, higher myocardial ATP levels and milder myocardial ultrastructural injury. There was no difference between the group Ⅰand Ⅱ. These results suggest that the aprotinin at a dose of 200 KIU/ml has no harmful effects on normally perfused hearts and has a marked myocardial protective effect on the prolonged myocardial ischemia when used in cold crystalloid cardioplegia.
基金This project was supported by a grant from the National Natural Science Foundation of China （No. 30460132）.
文摘Background Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels （KATe） were the end effectors of cardio-protection. But whether mitochondrial KATe plays an important role in hyperpolarizing cardioplegia is not apparent. The present study investigated the effect of hyperpolarizing cardioplegia containing pinacidil （a nonselective KATe opener） on ischemia/repeffusion injury in rat hearts, especially the role of mitochondrial KATe in pinacidil hyperpolarizing cardioplegia. Methods Sprague-Dawley rat hearts were Langendorff-perfused for 20 minutes with Krebs-Henseleit buffer at 37℃ before equilibration. Cardiac arrest was then induced in different treatments： there was no arrest and ischemia in the normal group, the control group were arrested by clamping the aorta, depolarizing caidioplegia （St. Thomas solution containing 16 mmol/L KCI） and hyperpolarizing cardioplegia groups used St. Thomas solution containing 0.05 mmol/L pinacidil and 5 mmol/L KCI to induce cardiac arrest in group hyperkalemic and group pinacidil, in group hyperkalemic ＋ 5-hydroxydecanote （5HD） and Pinacidil ＋ 5HD, 5HD （0.1 retool/L） was added to the above two solutions to block mitochondria KATe channels. Global ischemia was then administrated for 40 minutes at 37℃, followed by 30 minutes of reperfusion. At the end of equilibration and reperfusion, hemodynamics, ultrastructure, and mitochondrial function were measured. Results In the control group, ischemia/reperfusion decreased the left ventricular developed pressure, heart rate, coronary flow, mitochondrial membrane potential, impaired mitochondrial respiratory function, increased reactive oxygen species and left ventricular end diastolic pressure. Damage to myocardial ultrastructure was also evident. Both depolarized arrest and especially hyperpolarized cardioplegia significantly reduced these lesions. 5HD partially blocked the beneficial effects of pinacidil cardioplegia but showing no effects on hyperkalemic arrest. Conclusions Pinacidil cardioplegia provides better cardioprotection with preservation of hemodynamics, ultrastructure, and mitochondrial function than traditional cardioplegia. The mitochondria KATe channels may play an important role in the protection mechanism.
