Kanter K R, Flaherty J T, Bulkley B H, Gott V L, Gardner T J
Circulation. 1981 Aug;64(2 Pt 2):II84-90.
The use of propranolol with multidose potassium cardioplegia was studied in 32 in situ canine hearts subjected to 90 minutes of global ischemia at 15 degrees C and 60 minutes of reperfusion at 37 degrees C. All hearts received potassium (37 mEq/l) every 30 minutes during ischemia. There were four groups of equal size: group 1 received no propranolol, group 2 received low-dose propranolol and group 3 received high-dose propranolol. Group 4 received high-dose propranolol only with the initial potassium infusion. Myocardial CO2 (PmCO2) was monitored by mass spectrometry as an indicator of metabolic activity. An intraventricular balloon was used to measure isovolumic developed pressure, maximal dP/dt and end-diastolic pressure (EDP) before and after ischemia. During ischemia, peak PmCO2 was significantly higher in group 1 (45.6 +/- 2.8 mm Hg) than in groups 2, 3 and 4 (35.2 +/- 2.8 mm Hg, 33.4 +/- 2.8 mm Hg and 30.4 +/0 2.8 mm Hg, respectively) (p less than 0.05). There were no differences between the four groups in systolic ventricular function assessed by developed pressure and dP/dt. Hearts that received high-dose propranolol had significantly lower EDP after 60 minutes of reperfusion (group 3 13.3 +/- 1.5 mm Hg, group 4 10.4 +/0 1.5 mm Hg) compared with group 1 hearts (25.3 +/- 3.8 mm Hg, p less than 0.05). Hearts in groups 3 and 4 exhibited less ischemic injury as assessed by electron microscopy than hearts in groups 1 and 2. These data show that propranolol added to multidose potassium cardioplegia reduced metabolic activity during ischemia and improved ventricular compliance during reperfusion without depressing systolic function. Because left ventricular compliance and morphologic preservation were similar in groups 3 and 4, it appears that a single high dose of propranolol is sufficient and that subsequent doses do not further enhance the beneficial effects.
在32只原位犬心脏中研究了普萘洛尔与多剂量钾停搏液联合使用的情况,这些心脏在15℃下经历90分钟全心缺血,并在37℃下再灌注60分钟。所有心脏在缺血期间每30分钟接受一次钾(37 mEq/l)。分为四组,每组大小相等:第1组未接受普萘洛尔,第2组接受低剂量普萘洛尔,第3组接受高剂量普萘洛尔。第4组仅在初始钾输注时接受高剂量普萘洛尔。通过质谱法监测心肌二氧化碳(PmCO2)作为代谢活性指标。在缺血前后,使用心室内球囊测量等容收缩压、最大dP/dt和舒张末期压力(EDP)。在缺血期间,第1组的峰值PmCO2(45.6±2.8 mmHg)显著高于第2、3和4组(分别为35.2±2.8 mmHg、33.4±2.8 mmHg和30.4±2.8 mmHg)(p<0.05)。通过收缩压和dP/dt评估的四组心室收缩功能无差异。与第1组心脏(25.3±3.8 mmHg,p<0.05)相比,接受高剂量普萘洛尔的心脏在再灌注60分钟后EDP显著更低(第3组13.3±1.5 mmHg,第4组10.4±1.5 mmHg)。通过电子显微镜评估,第3组和第4组的心脏比第1组和第2组的心脏表现出更少的缺血损伤。这些数据表明,添加到多剂量钾停搏液中的普萘洛尔在缺血期间降低了代谢活性,并在再灌注期间改善了心室顺应性,而不降低收缩功能。由于第3组和第4组的左心室顺应性和形态学保存相似,似乎单次高剂量的普萘洛尔就足够了,后续剂量不会进一步增强有益效果。