Aoki M, Nomura F, Kawata H, Mayer J E
Department of Cardiovascular Surgery, Harvard Medical School, Boston, Mass.
J Thorac Cardiovasc Surg. 1993 Feb;105(2):207-12; discussion 212-3.
Hypothermia has been reported to increase intracellular ionized calcium, which may aggravate injury resulting from ischemia and reperfusion. The effects of plasma ionized calcium concentration ([Ca2+]) during hypothermic perfusion on recovery after 2 hours of cold cardioplegic ischemia were evaluated in 32 isolated, blood-perfused neonatal lamb hearts. Three groups of hearts (B, C, and D) were perfusion-cooled for 10 minutes to a myocardial temperature of 17 degrees C and then arrested with St. Thomas' Hospital cardioplegic solution. Group A had 10 minutes of normothermic perfusion before cardioplegia. Group B had cooling with normal [Ca2+]. Group C had citrate added as cooling was started to lower [Ca2+] (0.26 mmol/L), and it was not normalized until 15 minutes into reperfusion. Group D received citrate plus Ca2+ to give normal [Ca2+] during cooling. Groups B and D showed a significantly reduced recovery (p < 0.05) in left ventricular systolic function (developed pressure and the rate of pressure rise) and diastolic function (stiffness constant) than groups A and C. During preischemic cooling, oxygen consumption per beat and coronary vascular resistance increased significantly in groups B and D, but both oxygen consumption and coronary vascular resistance were significantly lower in group C than in groups B and D so long as [Ca2+] was low. The data show that preischemic hypothermia results in reduced postischemic recovery of function compared with simultaneous induction of cardioplegia and hypothermia. Low [Ca2+] during preischemic hypothermia and early reperfusion offsets this deleterious effect of hypothermia.
据报道，体温过低会增加细胞内游离钙，这可能会加重缺血再灌注造成的损伤。在32个离体、血液灌注的新生羔羊心脏中，评估了低温灌注期间血浆游离钙浓度（[Ca2+]）对冷停搏缺血2小时后恢复情况的影响。三组心脏（B组、C组和D组）灌注冷却10分钟，使心肌温度降至17摄氏度，然后用圣托马斯医院心脏停搏液使其停搏。A组在心脏停搏前进行10分钟的常温灌注。B组在正常[Ca2+]下冷却。C组在开始冷却时添加柠檬酸盐以降低[Ca2+]（0.26 mmol/L），直到再灌注15分钟时才恢复正常。D组在冷却期间接受柠檬酸盐加钙离子以使[Ca2+]正常。与A组和C组相比，B组和D组左心室收缩功能（发展压力和压力上升速率）和舒张功能（硬度常数）的恢复明显降低（p<0.05）。在缺血前冷却期间，B组和D组每搏耗氧量和冠状动脉血管阻力显著增加，但只要[Ca2+]较低，C组的耗氧量和冠状动脉血管阻力均显著低于B组和D组。数据表明，与同时诱导心脏停搏和低温相比，缺血前低温会导致缺血后功能恢复降低。缺血前低温和早期再灌注期间的低[Ca2+]可抵消低温的这种有害作用。
