Clark R E, Christlieb I Y, Ferguson T B, Weldon C S, Marbarger J P, Sobel B E, Roberts R, Henry P D, Ludbrook P A, Biello D, Clark B K
Ann Surg. 1981 Jun;193(6):719-32. doi: 10.1097/00000658-198106000-00007.
This report summarizes five years of laboratory investigations and the initial six-month clinical experience with a calcium antagonist, nifedipine, added to a cold hyperkalemic cardioplegic solution for enhancement of myocardial protection. Regional ischemia was created in 112 dogs and global ischemia in 98 dogs, under normothermic and two hyperthermic states. Control solutions, two clinical cardioplegic solutions, and nifedipine solutions were compared. Infusion of nifedipine during regional ischemia and reperfusion intervals resulted in a two-to-threefold reduction in injury volume and maintenance of normal left ventricular function in contrast infusion of nitroprusside. Nifedipine solutions (0.2 microgram/ml) provided superior preservation of left ventricular function in comparison to the two cardioplegic solutions after one hour of global ischemia at 37 degrees C and two hours at 18 C. In a clinical trial of nifedipine in cold potassium cardioplegia, 38 high risk patients with poor ventricular function have been treated; 22 of which were intensively studied serially with radionuclide ventriculography and pyrophosphate scans, myocardial isoenzyme determinations, 24 hour EKG recordings and intra- and postoperative hemodynamic studies. Of the 35 patients admitted to the intensive care unit (ICU), 33 have survived. Stroke work and cardiac indices return promptly to near normal levels after operation. The time-isoenzyme activity curves are low and radionuclide determined ejection fractions show no change for the study group. Death from acute postischemic cardiac failure did not occur in treated patients and the usage of intra-aortic balloon pump (IABP) has decreased threefold in comparison with 40 similar high risk patients treated concurrently with cardioplegic solution alone. It is concluded that nifedipine is a potent adjunct to cold hyperkalemic cardioplegic solution in high risk patients.
本报告总结了五年的实验室研究以及最初六个月使用钙拮抗剂硝苯地平添加到冷高钾心脏停搏液中以增强心肌保护的临床经验。在正常体温和两种高温状态下，对112只犬造成局部缺血，对98只犬造成全心缺血。比较了对照溶液、两种临床心脏停搏液和硝苯地平溶液。在局部缺血和再灌注期间输注硝苯地平导致损伤体积减少两到三倍，并维持正常左心室功能，相比之下输注硝普钠则不然。在37℃全心缺血1小时和18℃全心缺血2小时后，与两种心脏停搏液相比，硝苯地平溶液（0.2微克/毫升）能更好地保存左心室功能。在一项硝苯地平用于冷钾心脏停搏的临床试验中，38例心室功能较差的高危患者接受了治疗；其中22例通过放射性核素心室造影和焦磷酸盐扫描、心肌同工酶测定、24小时心电图记录以及术中和术后血流动力学研究进行了连续深入研究。在入住重症监护病房（ICU）的35例患者中，33例存活。术后每搏功和心脏指数迅速恢复到接近正常水平。研究组的时间-同工酶活性曲线较低，放射性核素测定的射血分数无变化。治疗患者未发生急性缺血后心力衰竭死亡，与单独使用心脏停搏液同时治疗的40例类似高危患者相比，主动脉内球囊泵（IABP）的使用减少了两倍。得出的结论是，硝苯地平是高危患者冷高钾心脏停搏液的有效辅助药物。
