Bodenhamer R M, DeBoer L W, Geffin G A, O'Keefe D D, Fallon J T, Aretz T H, Haas G S, Daggett W M
J Thorac Cardiovasc Surg. 1983 May;85(5):769-80.
To determine if, during elective cardiac arrest, the myocardial protection afforded by a cold (4 degrees C) crystalloid potassium cardioplegic solution could be improved by oxygenation of the solution, we placed 16 dogs on cardiopulmonary bypass and subjected their hearts to 4 hours of cold cardioplegic arrest. Group 1 hearts (n = 8) received aerated crystalloid solution perfused through the aortic root every 20 minutes. Group 2 hearts (n = 8) were treated identically except that the crystalloid cardioplegic solution was fully oxygenated. Left ventricular function curves (ejecting heart) were generated before arrest (control) and after 45 minutes of reperfusion. A cardiac output of 1,000 ml/min could be attained in only two hearts of Group 1 after reperfusion, whereas all but one heart of Group 2 had excellent functional preservation. Mean postreperfusion adenosine triphosphate (ATP) levels in Group 1 and Group 2 hearts were 62% and 89% of control, respectively (p less than 0.01). Myocardial water content had increased significantly (p less than 0.002) after reperfusion in Group 1, but not in Group 2. During cardioplegic solution infusion, myocardial oxygen consumption (MVO2) was 1.42 +/- 0.15 ml O2/min/100 gm LV for Group 1 and 6.91 +/- 1.27 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Oxygen consumed per minute of arrest was 0.027 +/- 0.003 ml O2/min/100 gm LV for Group 1 and 0.128 +/- 0.015 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Postreperfusion ultrastructural evaluation of two of the Group 1 hearts revealed severe ischemic damage in contrast to the normal ultrastructural appearance of two of the Group 2 hearts. With careful attention given to maintenance of myocardial hypothermia and cardioplegic delivery methods, the myocardial protection afforded by an oxygenated crystalloid cardioplegic solution exceeds that provided by the aerated control and compares favorably with other methods of myocardial protection during ischemic arrest.
为了确定在选择性心脏骤停期间，通过对冷（4摄氏度）晶体钾停搏液进行氧合是否可以改善其对心肌的保护作用，我们将16只狗置于体外循环下，使其心脏接受4小时的冷停搏液灌注停搏。第1组心脏（n = 8）每20分钟通过主动脉根部灌注充气晶体溶液。第2组心脏（n = 8）接受相同处理，只是晶体停搏液被充分氧合。在停搏前（对照）和再灌注45分钟后生成左心室功能曲线（跳动心脏）。再灌注后，第1组只有两颗心脏的心输出量能达到1000毫升/分钟，而第2组除一颗心脏外其余所有心脏的功能都得到了良好保留。第1组和第2组心脏再灌注后的平均三磷酸腺苷（ATP）水平分别为对照值的62%和89%（p < 0.01）。再灌注后，第1组心肌含水量显著增加（p < 0.002），而第2组没有。在灌注停搏液期间，第1组心肌耗氧量（MVO2）为1.42±0.15毫升O2/分钟/100克左心室，第2组为6.91±1.27毫升O2/分钟/100克左心室（p < 0.001）。第1组每停搏1分钟的耗氧量为0.027±0.003毫升O2/分钟/100克左心室，第2组为0.128±0.015毫升O2/分钟/100克左心室（p < 0.001）。对第1组两颗心脏进行再灌注后的超微结构评估显示有严重缺血损伤，而第2组两颗心脏的超微结构外观正常。在仔细注意维持心肌低温和停搏液输送方法的情况下，氧合晶体停搏液提供的心肌保护作用超过充气对照液，并且与缺血停搏期间的其他心肌保护方法相比具有优势。
