Habazettl H, Palmisano B W, Bosnjak Z J, Stowe D F
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Eur J Cardiothorac Surg. 1996;10(10):897-904. doi: 10.1016/s1010-7940(96)80318-6.
Initial warm cardioplegic reperfusion is widely used to ameliorate cardiac reperfusion damage after cardioplegic arrest. However, undesired effects of the high potassium concentration of the cardioplegic perfusate may limit the beneficial effect of this treatment. Contraction uncoupling by a negative inotropic and vasodilating agent such as 2,3-butanedione monoxime (BDM) may be superior to warm cardioplegic reperfusion in reducing reperfusion damage. Thus, initial reperfusion with BDM was compared with hyperkalemic reperfusion (HKR) after global ischemia of Langendorff-perfused guinea pig hearts.
Cardiac arrest was induced in 16 hearts using hyperkalemic Krebs' solution and hearts were stored unperfused at 37 degrees C for 40 min. Two groups were studied: HKR, initial reperfusion with 37 degrees C oxygenated hyperkalemic Krebs' for 5 min, and BDM, addition of 20 mM BDM to normokalemic Krebs' for 5 min.
BDM increased reactive coronary reflow (128 +/- 8%; all data mean +/- SEM of baseline) much more than HKR treatment (65 +/- 5%). O2 consumption was reduced more by HKR (28 +/- 1%) than by BDM (42 +/- 4%), but the O2 supply/consumption ratio was higher with BDM. During perfusion with normal Krebs' solution, flow stabilized at about 75% of baseline in both groups. Post-ischemic responses to adenosine, serotonin, and nitroprusside were depressed to a similar degree in both two groups. Recovery of left ventricular developed pressure was better in BDM (69 +/- 2%) than in HKR (61 +/- 3%)-treated hearts. Reperfusion dysrhythmias were markedly reduced after BDM reperfusion.
These data indicate that treatment in the initial 5-min reperfusion period with BDM is more effective than hyperkalemic reperfusion in reducing reperfusion damage.
初始温血心脏停搏液再灌注被广泛用于减轻心脏停搏后的心脏再灌注损伤。然而,心脏停搏灌注液的高钾浓度所带来的不良影响可能会限制这种治疗的有益效果。使用负性肌力和血管扩张剂(如2,3-丁二酮一肟,BDM)进行收缩解偶联在减轻再灌注损伤方面可能优于温血心脏停搏液再灌注。因此,将BDM初始再灌注与Langendorff灌注豚鼠心脏全心缺血后的高钾再灌注(HKR)进行了比较。
使用高钾Krebs溶液诱导16颗心脏停搏,并在37℃下无灌注保存40分钟。研究了两组:HKR组,用37℃含氧高钾Krebs溶液进行初始再灌注5分钟;BDM组,在正常钾Krebs溶液中加入20 mM BDM 5分钟。
BDM使反应性冠脉再灌注增加(128±8%;所有数据均为基线的平均值±标准误),比HKR治疗(65±5%)增加更多。HKR组(28±1%)比BDM组(42±4%)更多地降低了耗氧量,但BDM组的氧供/耗氧比更高。在用正常Krebs溶液灌注期间,两组的血流均稳定在基线的约75%。两组缺血后对腺苷、5-羟色胺和硝普钠的反应均受到相似程度的抑制。BDM治疗组(69±2%)左心室舒张末压的恢复比HKR治疗组(61±3%)更好。BDM再灌注后再灌注心律失常明显减少。
这些数据表明,在初始5分钟再灌注期用BDM治疗在减轻再灌注损伤方面比高钾再灌注更有效。