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首页> 外文期刊>The Annals of Thoracic Surgery: Official Journal of the Society of Thoracic Surgeons and the Southern Thoracic Surgical Association >The Myocardial Protection of Polarizing Cardioplegia Combined With Delta-Opioid Receptor Agonist in Swine
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The Myocardial Protection of Polarizing Cardioplegia Combined With Delta-Opioid Receptor Agonist in Swine

机译:猪极化极化停搏结合三角洲阿片受体激动剂的心肌保护

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StatisticsResultsThe purpose of this study was to determine whether polarized arrest using adenosine/lidocaine cold crystalloid cardioplegia in combination with the hibernation inductor δ-opioid receptor agonist pentazocine would give satisfactory myocardial protection rather than using depolarized supranormal potassium cardioplegia, supranormal potassium cardioplegia with pentazocine, or adenosine/lidocaine cardioplegia.MethodsTwenty pigs were randomly divided into four groups (n = 5 each) to receive the four types of cold crystalloid cardioplegia with an aortic cross-clamp time of 1 hour. Hemodynamic data were continuously measured, as was the left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP), plus or minus derivative of change in diastolic pressure over time (±dp/dt), cardiac output, pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac troponin I, and left ventricular ultrastructure.ResultsBoth the adenosine/lidocaine/pentazocine group and the adenosine/lidocaine group got significantly better results than the hyperkalemic and hyperkalemic pentazocine groups in improving hemodynamic values, pulmonary capillary wedge pressure, LVEDP, LVESP, ±dp/dt, cardiac output, cardiac troponin I values, and left ventricular ultrastructure. There were no statistical differences between the adenosine/lidocaine/pentazocine group and the adenosine/lidocaine group at 1 hour after cross-clamp removal; but at 2 hours after cross-clamp removal, the adenosine/lidocaine/pentazocine group stands out (LVEDP 3.3 ± 0.5, LVESP 122.5 ± 18.9, +dp/dt 2.9 ± 0.1, ?dp/dt 2.0 ± 0.6, cardiac output 2.6 ± 0.4, and troponin I 4.9 ± 0.5), with significant differences from the adenosine/lidocaine group (LVEDP 5.8 ± 1.0, LVESP 98.5 ± 10.1, +dp/dt 2.5 ± 0.2, ?dp/dt 1.0 ± 0.2, cardiac output 2.2 ± 0.2, troponin I 8.2 ± 0.8; p < 0.05). The defibrillation rate was largely decreased after the cross-clamp was released in the group containing pentazocine in cardioplegia.ConclusionsAdenosine/lidocaine/pentazocine cold crystalloid cardioplegia gave satisfactory cardiac arrest and better myocardial protection than the other three groups, especially with regard to improving prolonged postoperative cardiac function.Abbreviations and Acronyms: AL (adenosine/lidocaine), ALP (adenosine/lidocaine/pentazocine), ATP (adenosine triphosphate), CPB (cardiopulmonary bypass), cTnI (cardiac troponin I), dp/dt (derivative of change in diastolic pressure over time), K (hyperkalemic cardioplegia), KP (hyperkalemic cardioplegia with pentazocine), LVEDP (left ventricular end-diastolic pressure), LVESP (left ventricular end-systolic pressure), MAP (mean arterial pressure), PAP (pulmonary artery pressure)CTSNet classification:31Hyperkalemic cardioplegia (St. Thomas solution) has been the foundation of most myocardial protection strategies since its introduction more than 25 years ago. But apart from electrochemical arrest, these solutions are far from perfect. Myocardial membrane depolarization with potassium is associated with continued transmembrane ionic fluxes through sodium and calcium “window currents.” It gives ionic imbalance, intracellular sodium and calcium overload, and continued energy expenditure, which subsequently may cause contracture and myocardial injury. Cardiomyocyte dysfunction and death, microvascular injury, coronary vasoconstriction and spasm, arrhythmias, and left ventricular stunning [
机译:统计结果本研究的目的是确定使用腺苷/利多卡因冷晶体停搏结合冬眠诱导剂δ-阿片类受体激动剂喷他佐辛极化停搏是否能提供令人满意的心肌保护,而不是使用去极化超正常钾心停瘫,超正常钾心停搏联合喷他佐辛或方法将20只猪随机分为四组(每组5只),接受四种类型的冷结晶性心脏停搏,主动脉夹钳时间为1小时。连续测量血流动力学数据,包括左室舒张末期压力(LVEDP),左室收缩末期压力(LVESP),舒张压随时间的变化(±dp / dt),心输出量,结果,腺苷/利多卡因/喷他佐辛组和腺苷/利多卡因组在改善血流动力学值,肺毛细血管扩张方面均比高钾血症和高钾血症喷他辛胺组明显好楔形压力,LVEDP,LVESP,±dp / dt,心输出量,心肌肌钙蛋白I值和左心室超微结构。交叉钳清除后1小时,腺苷/利多卡因/喷他佐辛组与腺苷/利多卡因组之间无统计学差异。但是在十字夹钳移除后2小时,腺苷/利多卡因/喷他佐辛组表现出色(LVEDP 3.3±0.5,LVESP 122.5±18.9,+ dp / dt 2.9±0.1,Δdp/ dt 2.0±0.6,心输出量2.6± 0.4和肌钙蛋白I 4.9±0.5)与腺苷/利多卡因组有显着差异(LVEDP 5.8±1.0,LVESP 98.5±10.1,+ dp / dt 2.5±0.2,Δdp/ dt 1.0±0.2,心输出量2.2± 0.2,肌钙蛋白I 8.2±0.8; p <0.05)。含有戊唑辛的心脏停搏组中的交叉钳夹解除后,除颤率大大降低。结论腺苷/利多卡因/戊唑辛冷结晶性心脏停搏比其他三组具有令人满意的心脏停搏和更好的心肌保护作用,特别是在改善术后延长时间方面缩写:AL(腺苷/利多卡因),ALP(腺苷/利多卡因/喷他佐辛),ATP(三磷酸腺苷),CPB(体外循环),cTnI(心肌肌钙蛋白I),dp / dt(变化的衍生物)舒张压随时间的变化),K(高容量性心脏停搏),KP(含喷他佐汀的高容量性心脏停搏),LVEDP(左心室舒张末期压力),LVESP(左心室末末收缩压),MAP(平均动脉压),PAP(肺动脉压)自从CTSNet分类:31以来,高钾性心脏麻痹(圣托马斯溶液)一直是大多数心肌保护策略的基础它的推出已超过25年。但是,除了电化学抑制之外,这些解决方案还远非完美。钾使心肌膜去极化与通过钠和钙“窗电流”的持续跨膜离子通量有关。它会导致离子失衡,细胞内钠和钙超载以及持续的能量消耗,继而可能引起挛缩和心肌损伤。心肌细胞功能障碍和死亡,微血管损伤,冠状动脉血管收缩和痉挛,心律不齐和左室震颤[

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