EFFECTS OF MYOCARDIAL-ISCHEMIA ON THE RELEASE OF CARDIAC TROPONIN-I IN ISOLATED RAT HEARTS

Background: The twofold aim of this experimental study,vas fl) to veri fy the correlation between the duration of ischemia and concentration of cardiac troponin I and (2) to compare the release of cardiac tropon in I with histologic findings. Methods: Experiments were done on 18 ra t hearts, which were perfused according to the Langendorff method, imm ediately after excision in group I (control group) and after immersion for 3 hours (group II) and 6 hours (group III) in St. Thomas' Hospita l solution at 4 degrees C, During reperfusion, the release of cardiac troponin I, creatine kinase isoenzyme MB, and lactate dehydrogenase, t he recovery of left ventricular pressure, and heart rates were compare d among the three groups. After the experiment, three samples of myoca rdium (left ventricle, right ventricle, and septum) were taken for his tologic examination. Results: Cardiac troponin I concentration was sig nificantly 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 grou p to the other. Left ventricular pressure was not significantly differ ent 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. Conclusion: T his experimental study showed (1) that cardiac troponin I is an early marker of ischemic injury and (2) that cardiac troponin I concentratio n increases as the ischemic period increases. Early cardiac troponin I release appears to correlate with the extent of ischemic injury in ra ts undergoing buffer perfusion.