Misare B D, Krukenkamp I B, Lazer Z P, Levitsky S
Department of Surgery, Harvard Medical School, Boston, Mass.
J Thorac Cardiovasc Surg. 1993 Jan;105(1):37-44.
To assess the effectiveness of warm antegrade continuous blood cardioplegia in the setting of an acute coronary arterial occlusion, we instrumented 19 Yorkshire swine to quantitate left ventricular global, systolic, diastolic, and regional mechanics. Data were acquired before and after 10 minutes of mid-left anterior descending coronary artery occlusion followed by 60 minutes of aortic crossclamping. Cardiac arrest was induced by the antegrade infusion of 20 ml/kg of warm (37 degrees C) or cold (4 degrees C) oxygenated blood cardioplegic solution followed by either continuous warm (75 ml/min, n = 9) or intermittent cold (10 ml/kg every 20 minutes, n = 10) cardioplegic reinfusions. Left anterior descending coronary artery occlusion was released 20 minutes after aortic crossclamping and resulted in warm-arrested hearts developing a 139% increase in global oxygen consumption compared with values obtained with the left anterior descending coronary artery occluded (p < 0.02). Recovery of global left ventricle contractility, quantitated by the linear preload recruitable stroke-work relationship, was significantly worse after warm cardioplegia (52.4% +/- 5.1% versus 68.0% +/- 5.9%, warm versus cold, p < 0.05). Similarly, left anterior descending coronary artery regional ischemic zone contractility recovered 34.5% +/- 7.3% of control function with cold cardioplegia, whereas warm cardioplegia resulted in -11.36% +/- 7.46% functional recovery indicative of dyssynchronous contraction (p < 0.05). Diastolic compliance, calculated with an exponential end-diastolic pressure-versus-volume relationship, was not changed postischemically in either group. These data suggest that warm antegrade blood cardioplegia may potentiate acute ischemic injury and provide inadequate myocardial protection.
为评估温血顺行持续灌注心脏停搏液在急性冠状动脉闭塞情况下的有效性，我们对19只约克夏猪进行了仪器植入，以定量分析左心室整体、收缩、舒张和局部力学。在左前降支冠状动脉闭塞10分钟后，接着进行60分钟的主动脉交叉钳夹，分别在这两个阶段前后采集数据。通过顺行输注20ml/kg的温（37℃）或冷（4℃）氧合心脏停搏液诱导心脏停搏，随后分别进行持续温血（75ml/min，n = 9）或间断冷血（每20分钟10ml/kg，n = 10）心脏停搏液再灌注。在主动脉交叉钳夹20分钟后松开左前降支冠状动脉闭塞，结果显示，与左前降支冠状动脉闭塞时相比，温血停搏的心脏整体氧耗增加了139%（p < 0.02）。通过线性前负荷可募集搏功关系定量分析，温血心脏停搏后左心室整体收缩性的恢复明显较差（温血组为52.4%±5.1%，冷血组为68.0%±5.9%，p < 0.05）。同样，冷血心脏停搏时左前降支冠状动脉局部缺血区收缩性恢复至对照功能的34.5%±7.3%，而温血心脏停搏导致-11.36%±7.46%的功能恢复，提示收缩不同步（p < 0.05）。两组在缺血后通过指数型舒张末期压力-容积关系计算的舒张顺应性均未改变。这些数据表明，温血顺行灌注心脏停搏液可能会增强急性缺血损伤，提供的心肌保护不足。
