Kempsford R D, Hearse D J
Cardiovascular Research, Rayne Institute, St. Thomas' Hospital, London, England.
J Thorac Cardiovasc Surg. 1990 Feb;99(2):269-79.
There are conflicting reports of the detrimental or beneficial effects of hypothermic cardioplegia in the immature heart. We therefore investigated the temperature-dependence of myocardial protection and the ability of single-dose and multidose infusions of cardioplegic solution to protect the immature heart during hypothermic ischemia. Isolated, working hearts (n = 6 per group) from neonatal rabbits (aged 7 to 10 days) were perfused aerobically (37.0 degrees C) for 20 minutes before infusion (2 minutes) with either perfusion fluid (noncardioplegia control) or St. Thomas' Hospital cardioplegic solution and ischemic arrest (for 4, 6, and 18 hours) at various temperatures between 10.0 degrees and 30.0 degrees C. Hearts arrested with cardioplegic solution received either one preischemic infusion only (single-dose cardioplegia) or repeated infusions at intervals of 60 or 180 minutes (multidose cardioplegia). Ischemic arrest with single-dose cardioplegia for 4 hours at 10.0 degrees, 20.0 degrees, 22.5 degrees, 25.0 degrees, 27.5 degrees, and 30.0 degrees C resulted in 96.0% +/- 4.3%, 96.6 +/- 2.5%, 87.0% +/- 3.8%, 71.8% +/- 10.0% (p less than 0.05 versus 10.0 degrees C group), 35.1% +/- 10.3% (p less than 0.01 versus 10.0 degrees C group), and 3.0% +/- 1.9% (p less than 0.04 versus 10.0 degrees C group) recovery of preischemic cardiac output, respectively. With 6 hours of ischemia at 20.0 degrees C, single-dose cardioplegia significantly (p less than 0.01) increased the recovery of cardiac output from 20.9% +/- 13.1% (control) to 76.4% +/- 4.4%, whereas multidose cardioplegia (infusion every 60 minutes) further increased recovery to 97.8% +/- 3.8% (p less than 0.01 versus control and single-dose cardioplegia). In contrast, after 6 hours of ischemia at 10.0 degrees C, cardiac output recovered to 93.4% +/- 1.2% (control) and 92.3% +/- 3.1% (single-dose cardioplegia), whereas multidose cardioplegia reduced recovery to 76.9% +/- 2.2% (p less than 0.01 versus both groups). This effect was confirmed after 18 hours of ischemia at 10.0 degrees C; single-dose cardioplegia significantly increased the recovery of cardiac output from 24.5% +/- 10.9% (control) to 62.9% +/- 13.3% (p less than 0.05), whereas multidose cardioplegia reduced recovery to 0.8% +/- 0.4% (p less than 0.01 versus single-dose cardioplegia) and elevated coronary vascular resistance from 8.90 +/- 0.56 mm Hg.min/ml (control) to 47.83 +/- 9.85 mm Hg.min/ml (p less than 0.01). This effect was not reduced by lowering the infusion frequency (from every 60 to every 180 minutes).(ABSTRACT TRUNCATED AT 400 WORDS)
关于低温心脏停搏液对未成熟心脏的有害或有益作用,存在相互矛盾的报道。因此,我们研究了心肌保护的温度依赖性以及心脏停搏液单次和多次输注在低温缺血期间保护未成熟心脏的能力。从新生兔(7至10日龄)分离出工作心脏(每组n = 6),在灌注(2分钟)灌注液(非心脏停搏液对照)或圣托马斯医院心脏停搏液之前,在37.0℃下有氧灌注20分钟,并在10.0℃至30.0℃之间的不同温度下进行缺血性停搏(4、6和18小时)。用心脏停搏液停搏的心脏仅接受一次缺血前输注(单次剂量心脏停搏)或每隔60或180分钟重复输注(多次剂量心脏停搏)。在10.0℃、20.0℃、22.5℃、25.0℃、27.5℃和30.0℃下用单次剂量心脏停搏进行4小时缺血性停搏后,缺血前心输出量的恢复率分别为96.0%±4.3%、96.6±2.5%、87.0%±3.8%、71.8%±10.0%(与10.0℃组相比,p<0.05)、35.1%±10.3%(与10.0℃组相比,p<0.01)和3.0%±1.9%(与10.0℃组相比,p<0.04)。在20.0℃下缺血6小时,单次剂量心脏停搏显著(p<0.01)将心输出量的恢复率从20.9%±13.1%(对照组)提高到76.4%±4.4%,而多次剂量心脏停搏(每隔60分钟输注)进一步将恢复率提高到97.8%±3.8%(与对照组和单次剂量心脏停搏相比,p<0.01)。相比之下,在10.0℃下缺血6小时后的心输出量恢复率为93.4%±1.2%(对照组)和92.3%±3.1%(单次剂量心脏停搏),而多次剂量心脏停搏将恢复率降低到76.9%±2.2%(与两组相比,p<0.01)。在10.0℃下缺血18小时后证实了这种效果;单次剂量心脏停搏显著将心输出量的恢复率从24.5%±10.9%(对照组)提高到62.9%±13.3%(p<0.05),而多次剂量心脏停搏将恢复率降低到0.8%±0.4%(与单次剂量心脏停搏相比,p<0.01),并将冠状动脉血管阻力从8.90±0.56mmHg.min/ml(对照组)提高到47.83±9.85mmHg.min/ml(p<0.01)。降低输注频率(从每隔60分钟到每隔180分钟)并没有减少这种效果。(摘要截断于400字)