Chocron S, Alwan K, Toubin G, Kantelip B, Clement F, Kantelip J P, Etievent J P
Department of Thoracic and Cardiovascular Surgery, Saint-Jacques Hospital, Besançon, France.
J Thorac Cardiovasc Surg. 1996 Aug;112(2):508-13. doi: 10.1016/S0022-5223(96)70279-9.
The twofold aim of this experimental study was (1) to verify the correlation between the duration of ischemia and concentration of cardiac troponin I and (2) to compare the release of cardiac troponin I with histologic findings.
Experiments were done on 18 rat hearts, which were perfused according to the Langendorff method, immediately after excision in group I (control group) and after immersion for 3 hours (group II) and 6 hours (group III) in St. Thomas' Hospital solution at 4 degrees C. During reperfusion, the release of cardiac troponin I, creatine kinase isoenzyme MB, and lactate dehydrogenase, the recovery of left ventricular pressure, and heart rates were compared among the three groups. After the experiment, three samples of myocardium (left ventricle, right ventricle, and septum) were taken for histologic examination.
Cardiac troponin I concentration was significantly higher in group III than in groups I and II and in group II compared with group I. Cardiac troponin I concentration increased as the ischemic period increased. The relation between cardiac troponin I release and ischemic duration tended to be linear. Creatine kinase MB and lactate dehydrogenase concentrations did not differ from one group to the other. Left ventricular pressure was not significantly different among the groups. In the control group, no heart had more than 10% of the myocytes affected. One of six hearts in group II and three of six in group III had more than 10% of myocytes affected.
This experimental study showed (1) that cardiac troponin I is an early marker of ischemic injury and (2) that cardiac troponin I concentration increases as the ischemic period increases. Early cardiac troponin I release appears to correlate with the extent of ischemic injury in rats undergoing buffer perfusion.
本实验研究的双重目的是：（1）验证缺血持续时间与心肌肌钙蛋白I浓度之间的相关性；（2）比较心肌肌钙蛋白I的释放情况与组织学结果。
对18只大鼠心脏进行实验，按照Langendorff方法进行灌注。在第I组（对照组）中，心脏切除后立即进行灌注；在第II组中，心脏在4℃的圣托马斯医院溶液中浸泡3小时后进行灌注；在第III组中，心脏在4℃的圣托马斯医院溶液中浸泡6小时后进行灌注。在再灌注期间，比较三组中心肌肌钙蛋白I、肌酸激酶同工酶MB和乳酸脱氢酶的释放情况、左心室压力的恢复情况以及心率。实验结束后，取三份心肌样本（左心室、右心室和室间隔）进行组织学检查。
第III组中心肌肌钙蛋白I浓度显著高于第I组和第II组，且第II组高于第I组。心肌肌钙蛋白I浓度随着缺血时间的延长而增加。心肌肌钙蛋白I释放与缺血持续时间之间的关系呈线性趋势。肌酸激酶同工酶MB和乳酸脱氢酶浓度在各组之间无差异。各组之间左心室压力无显著差异。在对照组中，没有心脏的受影响心肌细胞超过10%。第II组的6只心脏中有1只、第III组的6只心脏中有3只的受影响心肌细胞超过10%。
本实验研究表明：（1）心肌肌钙蛋白I是缺血性损伤的早期标志物；（2）心肌肌钙蛋白I浓度随着缺血时间的延长而增加。在接受缓冲液灌注的大鼠中，早期心肌肌钙蛋白I的释放似乎与缺血性损伤的程度相关。
