Aoki M, Kawata H, Mayer J E
Department of Cardiovascular Surgery, Children's Hospital, MA 02115.
Circulation. 1992 Nov;86(5 Suppl):II346-51.
Hypothermic cardioplegia generally improves the recovery of the mechanical function of the heart after ischemia, but some components of cold cardioplegia may produce endothelial injury that can offset the protective effects of cardioplegia. This study was undertaken to evaluate the effect of extremely hypothermic cardioplegia on the recovery of coronary endothelial and cardiac mechanical function after ischemia in the immature heart.
Three groups of eight isolated, blood-perfused, neonatal lamb hearts each had myocardial temperature maintained at 10 degrees C during 2 hours of global ischemia but received hourly doses of crystalloid cardioplegic solution at temperatures of 10 degrees C (group A), 4 degrees C (group B), and 2 degrees C (group C). The percent recovery of isovolumic left ventricular maximum developed pressure in groups A (86.6 +/- 7.7) and B (90.5 +/- 7.5) was higher than in group C (78.6 +/- 6.3), and maximum dP/dt in groups A (89.6 +/- 8.6) and B (89.5 +/- 5.7) was higher than in group C (79.4 +/- 9.0) at 30 minutes of reperfusion (p < 0.05). Groups A (136.8 +/- 20.9) and B (142.8 +/- 27.7) achieved higher recovery of coronary blood flow (as percentage of baseline) at 15-minute reperfusion than group C (108.5 +/- 26.2), and myocardial oxygen consumption was higher in groups A (68.3 +/- 14.6, 92.1 +/- 21.1) and B (68.8 +/- 19.9, 85.3 +/- 25.5) than in group C (46.3 +/- 14.7, 57.2 +/- 14.2) at 15 and 30 minutes of reperfusion, respectively (p < 0.05). Percent recovery of the coronary vascular resistance responses to 10(-7) M concentration of an endothelium-dependent vasodilator (acetylcholine) in groups A (71.9 +/- 9.0) and B (66.2 +/- 23.1) was higher than in group C (24.2 +/- 14.3) (p < 0.05), whereas responses to 3 x 10(-5) M concentration of endothelium-independent vasodilator (nitroglycerin) were the same.
Excessively cold cardioplegic solution may cause endothelial dysfunction (reduced acetylcholine response) and reduced recovery of mechanical function in the neonatal heart.
低温心脏停搏通常可改善缺血后心脏机械功能的恢复，但冷心脏停搏的某些成分可能会导致内皮损伤，从而抵消心脏停搏的保护作用。本研究旨在评估极低温心脏停搏对未成熟心脏缺血后冠状动脉内皮和心脏机械功能恢复的影响。
三组，每组八颗离体、血液灌注的新生羔羊心脏，在2小时全心缺血期间将心肌温度维持在10℃，但分别接受每小时一剂温度为10℃（A组）、4℃（B组）和2℃（C组）的晶体心脏停搏液。再灌注30分钟时，A组（86.6±7.7）和B组（90.5±7.5）的等容左心室最大发育压力恢复百分比高于C组（78.6±6.3），A组（89.6±8.6）和B组（89.5±5.7）的最大dP/dt高于C组（79.4±9.0）（p<0.05）。再灌注15分钟时，A组（136.8±20.9）和B组（142.8±27.7）的冠状动脉血流恢复率（占基线的百分比）高于C组（108.5±26.2），再灌注15分钟和30分钟时，A组（68.3±14.6，92.1±21.1）和B组（68.8±19.9，85.3±25.5）的心肌氧耗高于C组（46.3±14.7，57.2±14.2）（p<0.05）。A组（71.9±9.0）和B组（66.2±23.1）对10⁻⁷M浓度的内皮依赖性血管扩张剂（乙酰胆碱）的冠状动脉血管阻力反应恢复百分比高于C组（24.2±14.3）（p<0.05），而对3×10⁻⁵M浓度的非内皮依赖性血管扩张剂（硝酸甘油）的反应相同。
过冷的心脏停搏液可能导致新生儿心脏内皮功能障碍（乙酰胆碱反应降低）和机械功能恢复降低。
