Time-course of cardiac troponin I release from isolated perfused rat hearts during hypoxia reoxygenation and ischemia reperfusion

The study was designed to determine the time-course of cardiac troponin I ( cTn-I) release in isolated and Langendorff-perfused rat hearts during hypox ia and reoxygenation (H/Reox), and after various durations of total ischemi a and subsequent reperfusion (I/R). For this purpose, in H/Reox, cTn-I was measured with the conventional Access(R) immunoassay (ng/ml) and a new immu noassay which operates at pg/ml, and compared with creatine kinase (CK), la ctate dehydrogenase (LD) and cardiac troponin T (cTn-T). In I/R, cTn-I was compared with CK and LD. The anti-Tn-I mAbs used in cTn-I assays cross-reac t with cTn-I: of the rat. A clear difference between time-courses and conce ntration levels of cTn-I in I/R and H/Reox models was found. In I/R, maximu m release of cTn-I, CK and LD similarly occurred within minutes following r eperfusion; however cTn-I did not return to baseline values. cTn-I levels w ere not linked to the duration of ischemia. In I/R, we were only able to de tect small cTn-I concentrations. In H/Reox experiments, cTn-I, CK and LD in creased time-dependently. We found higher cTn-I maximal peak levels detecte d with the Access(R) immunoassay than with the new assay (median, 0.346 ng/ ml per min/g dry wt. vs 132 pg/ml per min/g dry wt). cTn-T maximal concentr ations were lower than maximal cTn-I levels (median, 0.117 ng/ml per min/g dry wt). Time-courses of cTn-I release were roughly similar with both assay s in the H/Reox model (r = 0.90). These data indicate that the cTn-I time-c ourse is related to experimental model (I/R or N/Reox), but also likely dep ends on the sensitivity of cTn-I assays in such experimental conditions. (C ) 1999 Elsevier Science B.V. All rights reserved.