(Circulation. 1997;96:2414-2420.)
© 1997 American Heart Association, Inc.
Articles |
Right and Left Myocardial Antioxidant Responses During Heart Failure Subsequent to Myocardial Infarction
From the Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Correspondence to Dr Pawan K. Singal, Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, 351 Tache Ave, Room R3022, Winnipeg, Manitoba R2H 2A6, Canada. E-mail psingal{at}sbrc.umanitoba.ca
Background Heart failure subsequent to myocardial infarction (MI) is accompanied by depressed antioxidants and increased oxidative stress in the myocardium. Antioxidant enzyme activities and oxidative stress were examined in the viable left (LV) and right (RV) ventricles in relation to their hemodynamic function.
Methods and Results The left coronary artery in
rats was ligated. At 1 week after MI, LV systolic pressure
(LVSP), LV end-diastolic pressure (LVEDP), and RV
end-diastolic pressure (RVEDP) remained near control
values, whereas RV systolic pressure (RVSP) was significantly
elevated. In the 4, 8, and 16 week post-MI animals, LVSP was
significantly reduced, with values of 112.0±1.57, 99.9±0.52, and
89.2±1.4 mm Hg, whereas LVEDP was significantly elevated, with
values of 8.2±0.52, 17.4±1.7, and 31.4±1.5 mm Hg,
respectively. RVEDP was higher at 8 and 16 weeks, and RVSP was
significantly reduced at 16 weeks. At 1 week after MI, myocardial
catalase activity in the LV was maintained near control levels, whereas
in the RV, it was 134% compared with its control value. At 4, 8, and
16 weeks, catalase activity in the LV was 71%, 48%, and 28% of
respective controls. Catalase activity in the RV was significantly
reduced only at 16 weeks. A similar trend was seen with respect to
glutathione peroxidase activity. Reduced/oxidized glutathione ratio was
significantly depressed in the LV at 1, 4, 8, and 16 weeks, whereas in
the RV, this ratio was significantly reduced only at 8 and 16 weeks.
Myocardial lipid peroxidation in the LV at 4, 8, and 16 weeks was
elevated by 
40%, 51%, and 100%, respectively, whereas in the RV,
an increase of 50% was seen only at 16 weeks.
Conclusions These data show that heart failure subsequent to MI is associated with an antioxidant deficit as well as increased oxidative stress, first in the LV, followed by the RV. Furthermore, these changes correlated with the hemodynamic function in each of the ventricles, suggesting their role in the pathogenesis of ventricular dysfunction.
Key Words: heart failure • antioxidants • myocardial infarction • free radicals
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