Absence of troponin I degradation or altered sarcoplasmic reticulum uptakeprotein expression after reversible ischemia in swine

The findings of troponin I (TnI) proteolysis tin isolated rat hearts) and i nduction of selected sarcoplasmic reticulum (SR) calcium-regulatory genes ( after repetitive total coronary occlusions in swine) have given rise to the hypothesis that the time course of functional recovery of stunned myocardi um reflects the resynthesis of reversibly damaged proteins. Although stunni ng occurs after brief total occlusions and prolonged partial occlusions tie , short-term hibernation), the time course of functional recovery varies fr om a few hours to several days, suggesting that the severity of protein dam age or mechanisms responsible for the dysfunction may differ. To study this , we examined SR gene expression and TnI degradation in stunned myocardium produced by 10-minute total left anterior descending coronary artery (LAD) occlusions (n=4) or 1-hour partial LAD occlusions, in which now was reduced to approximate to 50% of control values for 60 minutes (n=6) in swine. One hour after reperfusion, LAD wall thickening was severely depressed in both models despite normal perfusion and no triphenyltetrazolium chloride evide nce of necrosis. Normal myocardium exhibited TnI immunoreactivity at 31 kDa and a weak secondary band at 27 kDa. Irreversible injury or calpain activa tion in vitro produced a marked increase in the intensity of the 27-kDa ban d, consistent with TnI degradation. Stunned myocardium demonstrated no chan ge in the 31- or the 27-kDa band, and the percentage of the 27- to 31-kDa b and remained constant after 10-minute total occlusions (LAD, 5.9+/-0.9%; no rmal, 4.9+/-1.6%) and 1-hour partial occlusions (LAD, 8.5+/-1.9%; normal, 7 .3+/-1.4%) and in sham controls (LAD, 10.9+/-1.5%; normal, 9.8+/-1.4%). Nor thern analysis showed no alterations in TnI or SR gene expression, but the stress protein HSP-70 was variably induced. Thus, stunned myocardium occurs without TnI degradation or altered SR gene expression, indicating that add itional mechanisms are responsible for the reversible dysfunction after sin gle episodes of regional ischemia in swine.