Summary
Changes in oxidative stress as indicated by the redox ratio as well as lipid peroxidation were characterized in rat hearts at different time points, subsequent to myocardial infarction (MI). In the severe heart failure stage at 16 weeks of post-MI, oxidative stress was significantly increased. Treatment with afterload reducing drugs, captopril or prazosin, started at 4 weeks post-MI and continued up to 16 weeks, resulted in a significant modulation of the oxidative stress changes with an improved hemodynamic function. It is suggested that the improved prognosis in MI patients with afterload reduction reported earlier may involve an improvement of the antioxidant reserve coupled with a reduction in the oxidative stress in the infarcted heart.
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Khaper, N., Hill, M.F., Pichardo, J., Singal, P.K. (1998). Effects of Captopril on Myocardial Oxidative Stress Changes in Post-Mi Rats. In: Dhalla, N.S., Zahradka, P., Dixon, I.M.C., Beamish, R.E. (eds) Angiotensin II Receptor Blockade Physiological and Clinical Implications. Progress in Experimental Cardiology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5743-2_39
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DOI: https://doi.org/10.1007/978-1-4615-5743-2_39
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