Jakobsen Øyvind, Muller Stig, Aarsaether Erling, Steensrud Tor, Sørlie Dag G
Department of Cardiothoracic and Vascular Surgery, University Hospital of North Norway and Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway.
Eur J Cardiothorac Surg. 2007 Sep;32(3):493-500. doi: 10.1016/j.ejcts.2007.05.020. Epub 2007 Jul 5.
To determine whether adenosine instead of supranormal potassium in cold crystalloid cardioplegia gives satisfactory cardiac arrest and improved cardioprotection. Cold crystalloid cardioplegia with adenosine, procaine and magnesium (A) was compared with standard cold crystalloid hyperkalemic cardioplegia (K).
Sixteen pigs were randomized to receive either cold K (n=8) or A (n=8), where hyperkalemia was substituted with 1.2 mM adenosine. The cold (6 degrees C) cardioplegia was given intermittently and antegradely, with an aortic cross-clamp time of 1 h. Hemodynamic data was continuously measured and pressure-volume conductance catheters were used to determine global left ventricular systolic and diastolic function. Coronary flow and O2 content differences allowed determination of left ventricular energetics. Blood samples, and left ventricular microdialysis were used to measure parameters of ischemia. Measurements were done at 1 and 2 h after cross-clamp release.
Mean arterial pressure was reduced with 55 mmHg (standard deviation, SD: 19) in the K group versus 30 mmHg (SD: 14) in the A group 2 h after cross-clamp release (p=0.030). Left ventricular contractility expressed as slope of the preload recruitable stroke work index (Mw) was reduced to 53% (SD: 14) in the K group versus 78% (SD: 23) in the A group 2h after cross-clamp release (p=0.046). Reduction of maximum of first derivate of pressure with respect to time (dP/dtmax) was 804 mmHg/s (SD: 189) in the K group versus 538 mmHg/s (SD: 184) in the A group (p=0.033). The slope of the myocardial oxygen consumption-pressure volume area was at 2 h reperfusion increased from 1.37 (SD: 0.64) to 2.86 (SD: 1.27) in the K group, whereas no shift was detected in the A group (p=0.019). Cardiac troponin T measured in the coronary sinus 1 h after cross-clamp release was 1.25 microg/l (SD: 0.64) in the K group versus 0.73 microg/l (SD: 0.31) in the A group (p=0.046).
Adenosine instead of supranormal potassium in cold crystalloid cardioplegia gives satisfactory cardiac arrest, improves post cardioplegic left ventricular systolic function and efficiency, and attenuates myocardial cell damage.
确定在冷晶体心脏停搏液中使用腺苷而非超正常钾是否能实现满意的心脏停搏并增强心脏保护作用。将含腺苷、普鲁卡因和镁的冷晶体心脏停搏液(A组)与标准冷晶体高钾心脏停搏液(K组)进行比较。
16头猪被随机分为两组,分别接受冷K组(n = 8)或A组(n = 8)处理,其中用1.2 mM腺苷替代高钾。冷(6℃)心脏停搏液采用间歇性顺行灌注,主动脉阻断时间为1小时。连续测量血流动力学数据,并使用压力 - 容积导管测定左心室整体收缩和舒张功能。通过冠状动脉血流和氧含量差异来确定左心室能量代谢。采集血样及进行左心室微透析以测量缺血参数。在松开主动脉阻断钳1小时和2小时后进行测量。
松开主动脉阻断钳2小时后,K组平均动脉压降低55 mmHg(标准差,SD:19),而A组降低30 mmHg(SD:14)(p = 0.030)。以预负荷可募集搏功指数(Mw)斜率表示的左心室收缩力,在松开主动脉阻断钳2小时后,K组降至53%(SD:14),而A组为78%(SD:23)(p = 0.046)。K组压力对时间的一阶导数最大值(dP/dtmax)降低为804 mmHg/s(SD:189),而A组为538 mmHg/s(SD:184)(p = 0.033)。在再灌注2小时时,K组心肌氧耗 - 压力容积面积斜率从1.37(SD:0.64)增加到2.86(SD:1.27),而A组未检测到变化(p = 0.019)。松开主动脉阻断钳1小时后,在冠状窦测量的心肌肌钙蛋白T,K组为1.25 μg/l(SD:0.64),而A组为0.73 μg/l(SD:0.31)(p = 0.046)。
在冷晶体心脏停搏液中使用腺苷而非超正常钾可实现满意的心脏停搏,改善心脏停搏后左心室收缩功能和效率,并减轻心肌细胞损伤。