Carrier M, Trudelle S, Khalil A, Pelletier L C
Department of Surgery, Université de Montréal, Que.
Can J Surg. 1998 Apr;41(2):142-8.
To study the changes in myocardial tissue pH and PO2 during cold- and warm-blood cardioplegic arrests.
An experimental study in dogs.
Nine dogs underwent the following procedures: 30 minutes with an empty heart beating under cardiopulmonary bypass (control period); 30 minutes of warm (33 degrees C) cardioplegic arrest with a 1:4 mix of crystalloid in blood solution administered continuously at 150 mL/min; 30 minutes of cold (15 degrees C) cardioplegic arrest; and 30 minutes of myocardial reperfusion. The cardioplegic blood solution was administered antegradely through the ascending aorta.
Tissue pH and PO2. Arterial and coronary sinus oxygen content and myocardial consumption calculated.
There was a modest but significant increase in the left anterior descending (LAD) and circumflex (Cx) tissue pH throughout the experiment. PmO2 in the LAD territory averaged 44 (7) mm Hg (mean and standard error of the mean) during the bypass period, 123 (23) mm Hg at the termination of warm cardioplegic arrest, 146 (28) mm Hg at the end of cold arrest and 66 (17) mm Hg after reperfusion. Oxygen consumption averaged 0.65 (0.15) mL/min during the bypass period, 0.3 (0.18) mL/min at the end of warm arrest, 0.25 (0.16) mL/min at the end of cold arrest and 0.45 (0.08) mL/min after reperfusion (p < 0.05). Oxygen delivery to the LAD territory was greater than myocardial oxygen consumption by an average of 2.02 (0.4) mL/min during bypass, 2.02 (0.62) mL/min after warm arrest, 2.12 (0.5) mL/min after cold arrest and 1.55 (0.25) mL/min after reperfusion (p > 0.05).
During cardioplegic arrest, tissue PO2 increased and oxygen consumption decreased significantly, whereas tissue pH remained normal, suggesting that continuous warm- and cold-blood cardioplegia maintained aerobic glycolysis during myocardial arrest. Thus, the increase in myocardial tissue PmO2 during cardioplegic arrest reflects the decrease in myocardial oxygen consumption while maintaining oxygen supply.
研究冷血和温血心脏停搏期间心肌组织pH值和PO₂的变化。
在犬类动物上进行的实验研究。
9只犬接受以下操作:在体外循环下空心跳动30分钟(对照期);以150 mL/分钟的速度持续输注含1:4晶体液的血液溶液,进行30分钟的温血(33℃)心脏停搏;进行30分钟的冷血(15℃)心脏停搏;以及30分钟的心肌再灌注。心脏停搏血液溶液经升主动脉顺行给药。
组织pH值和PO₂。计算动脉和冠状窦氧含量以及心肌耗氧量。
在整个实验过程中,左前降支(LAD)和回旋支(Cx)组织pH值有适度但显著的升高。在体外循环期间,LAD区域的PmO₂平均为44(7)mmHg(均值和均值标准误差),在温血心脏停搏结束时为123(23)mmHg,在冷血停搏结束时为146(28)mmHg,再灌注后为66(17)mmHg。在体外循环期间,氧耗量平均为0.65(0.15)mL/分钟,在温血停搏结束时为0.3(0.18)mL/分钟,在冷血停搏结束时为0.25(0.16)mL/分钟,再灌注后为0.45(0.08)mL/分钟(p<0.05)。在体外循环期间,输送至LAD区域的氧比心肌耗氧量平均多2.02(0.4)mL/分钟,在温血停搏后多2.02(0.62)mL/分钟,在冷血停搏后多2.12(0.5)mL/分钟,再灌注后多1.55(0.25)mL/分钟(p>0.05)。
在心脏停搏期间,组织PO₂升高,氧耗量显著降低,而组织pH值保持正常,这表明持续的温血和冷血心脏停搏在心肌停搏期间维持了有氧糖酵解。因此,心脏停搏期间心肌组织PmO₂的升高反映了心肌耗氧量的降低,同时维持了氧供应。