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  • Title: Post-ischaemic dysfunction does not correlate with release of cardiac troponin T in isolated rat hearts.
    Author: Kawakami T, Löwbeer C, Valen G, Vaage J.
    Journal: Acta Physiol Scand; 1999 Sep; 167(1):23-7. PubMed ID: 10519973.
    Abstract:
    Cardiac troponin T (cTnT) is a highly sensitive and specific serum marker of irreversible cardiomyocyte injury. It is not clear whether cTnT also is a suitable marker of subtle, reversible injury. In the present investigation the relationship between cTnT release and function during the first 30 min of reperfusion after 30 min of global ischaemia, was investigated in isolated, retrogradely perfused rat hearts. Left ventricular systolic (LVSP), end-diastolic (LVEDP) and developed (LVDP) pressures, heart rate (HR), and coronary flow (CF) were measured. In one series of experiments (n=7) the kinetics of cTnT release during 30 min of reperfusion was investigated. An early, short-lasting peak of cTnT release appeared after 30 s of reperfusion. Then cTnT release gradually increased with a maximum after 20 min (from 0.08 +/- 0.03 before ischaemia to 2.16 +/- 0.40 ng min-1) (mean +/- SEM). In a second series of experiments (n=52) the relationship between cTnT release and cardiac function was investigated after 20 min of reperfusion. At this time point LVEDP increased (0 to 62 +/- 3 mmHg) and LVDP decreased (84 +/- 2 to 33 +/- 3 mmHg), but without any correlation with cTnT release. cTnT release was positively correlated to LVSP (P < 0.04, r=0.29), and negatively correlated to HR (P < 0.03, r=-0.31). cTnT concentration in the coronary effluent increased in parallel to increasing CF (P < 0.03, r=0.31). In conclusion, during the early reperfusion period there was no consistent correlation between cTnT release and dysfunction after global ischaemia in the isolated rat heart. Release of cTnT and post-ischaemic function appear to provide supplementary information in this particular model.
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