Ellis R J, Pryor W, Ebert A
Ann Thorac Surg. 1977 Oct;24(4):229-306. doi: 10.1016/s0003-4975(10)63404-2.
An attempt was made to determine the effect of hypothermic potassium cardioplegia (35 mEq of potassium chloride) on the hypertrophic ventricle. Puppies with induced left ventricular hypertrophy were divided into four groups and studied after one hour on global ischemia. Myocardial adenosine triphosphate (ATP) was best preserved in the hypothermically perfused groups and correlated well with measurements of coronary sinus creatine phosphokinase (CPK). In Groups 1 and 2 (anoxic arrest at 37 degrees C and KC1 perfusion at 37 degrees C), CPK at 30 minutes of reperfusion was 1,031 and 198 IU, respectively, compared to 35 IU in Group 3 (KC1 perfusion at 4 degrees C) and 44 IU in Group 4 (Ringer's lactate at 4 degrees C). Myocardial injury was milder in Groups 3 and 4 regardless of whether potassium chloride was added. It is apparent that hypothermic perfusion of a hypertrophic ventricle was the major factor in myocardial preservation, as determined by myocardial ATP and coronary sinus CPK.
研究试图确定低温钾停搏液(含35毫当量氯化钾)对肥厚心室的影响。将诱导产生左心室肥厚的幼犬分为四组,在全心缺血1小时后进行研究。心肌三磷酸腺苷(ATP)在低温灌注组中保存得最好,且与冠状窦肌酸磷酸激酶(CPK)的测量结果相关性良好。在第1组和第2组(37℃无氧停搏和37℃氯化钾灌注)中,再灌注30分钟时的CPK分别为1031和198国际单位,而第3组(4℃氯化钾灌注)为35国际单位,第4组(4℃乳酸林格液灌注)为44国际单位。无论是否添加氯化钾,第3组和第4组的心肌损伤都较轻。显然,根据心肌ATP和冠状窦CPK测定,肥厚心室的低温灌注是心肌保存的主要因素。