Swanson D K, Myerowitz P D
J Thorac Cardiovasc Surg. 1983 Aug;86(2):242-51.
Reperfusion conditions significantly affect recovery following global myocardial ischemia. Using an isolated dog heart model, we investigated the effect of initial (first 10 minutes) reperfusion temperature and pressure on the metabolic and functional recovery of the preserved heart. Four groups of five or six dogs each underwent 2 hours of ischemic cardioplegic arrest at 15 degrees C following single-dose crystalloid cardioplegia. Hearts were initially reperfused at 37 degrees C (high temperature) or 28 degrees C (low temperature) and at 50 mm Hg (low pressure) or 80 mm Hg (high pressure), giving four groups: (1) high-temperature, high-pressure; (2) high-temperature, low-pressure; (3) low-temperature, high-pressure; and (4) low-temperature, low-pressure. Septal temperatures were continuously recorded. Ventricular function curves 1 and 2 hours following reperfusion were significantly depressed in the high-temperature, high-pressure group (70%, p less than 0.01, and 83%, p less than 0.02) and the low-temperature, high-pressure group (78%, p less than 0.03, and 85%, p less than 0.03) but were normal in the low-temperature, low-pressure and the high-temperature, low-pressure groups. All groups showed edema 1/2 hour after reperfusion as measured by water and sodium content in myocardial biopsy specimens but only the high-temperature, high-pressure and the low-temperature, high-pressure groups showed persistent edema at 3 hours (3.95 +/- 0.2 ml H2O/gm dry weight, p less than 0.03 and 3.99 +/- 0.16 ml/gm, p less than 0.02, respectively). Only low-temperature, high-pressure reperfusion resulted in statistically significant reductions in adenosine triphosphate (ATP) 1/2 hour and 2 hours following reperfusion (a 15% reduction from baseline). Maximum rewarming rates were measured for each group. High-temperature, high-pressure = 2 degrees C per second; low-temperature, high-pressure = 1 degree C per second; high-temperature, low-pressure = 0.75 degrees C per second; and low-temperature, low-pressure = 0.4 degrees C per second. High-pressure reperfusion following global myocardial ischemia results in rapid rewarming and is associated with prolonged myocardial edema, depressed ATP levels, and delayed functional recovery. Therefore, we employ 10 minutes of low-pressure reperfusion in our patients undergoing potassium cardioplegic arrest.
再灌注条件对全心缺血后的恢复有显著影响。我们使用离体犬心模型,研究了初始(最初10分钟)再灌注温度和压力对保存心脏的代谢及功能恢复的影响。每组五只或六只犬,共四组,在单剂量晶体心脏停搏液后于15℃进行2小时的缺血性心脏停搏。心脏最初分别在37℃(高温)或28℃(低温)以及50mmHg(低压)或80mmHg(高压)下再灌注,分为四组:(1)高温、高压;(2)高温、低压;(3)低温、高压;(4)低温、低压。持续记录室间隔温度。再灌注1小时和2小时后的心室功能曲线在高温、高压组(分别为70%,p<0.01;83%,p<0.02)和低温、高压组(分别为78%,p<0.03;85%,p<0.03)显著降低,但在低温、低压组和高温、低压组正常。通过心肌活检标本中的水和钠含量测量,所有组在再灌注半小时后均出现水肿,但只有高温、高压组和低温、高压组在3小时时仍有持续性水肿(分别为3.95±0.2ml H2O/g干重,p<0.03;3.99±0.16ml/g,p<0.02)。只有低温、高压再灌注在再灌注半小时和2小时后导致三磷酸腺苷(ATP)有统计学意义的降低(较基线降低15%)。测量了每组的最大复温速率。高温、高压组=每秒2℃;低温、高压组=每秒1℃;高温、低压组=每秒0.75℃;低温、低压组=每秒0.4℃。全心缺血后的高压再灌注导致快速复温,并伴有心肌水肿延长、ATP水平降低和功能恢复延迟。因此,我们在接受钾诱导心脏停搏的患者中采用10分钟的低压再灌注。