Abstract

Objectives: Menopause has a negative effect on cardiovascular functions. However, very little is known of the overall effect of menopause on the cardiac ultrastructure or the pathophysiological basis of this. Methods: A group of 12-week-old female Sprague Dawley rats were randomly allocated to healthy control (n = 6) and ovariectomy groups (n = 6). Twelve weeks after ovariectomy, the rats’ cardiac tissues were histopathologically analyzed for determination of oxidant and antioxidant enzymes [activities of catalase (CAT), superoxide dismutase (SOD), and myeloperoxidase (MPO) and amount of glutathione (GSH) and lipid peroxidation (LPO)]. Results: When compared to the control group, the ovariectomy group showed cardiomyopathic changes. In tissue, activities of CAT (185 ± 2.4 vs. 112 ± 1.4 mmol/min/mg tissue; p < 0.05), SOD (153 ± 1.0 vs. 146 ± 0.7 mmol/min/mg tissue; p < 0.05) and MPO (19 ± 0.8 vs. 8.6 ± 0.11 µmol/min/mg tissue; p < 0.05) and LPO levels (32.1 ± 0.77 vs. 14.4 ± 0.20 nmol/g tissue; p < 0.05) were significantly increased in the ovariectomy group when compared to the control group. However, GSH levels (3.43 ± 0.02 vs. 3.73 ± 0.01 nmol/g tissue; p < 0.05) were significantly lower in the ovariectomy group when compared to the control group. Conclusion: Using an experimental animal model, we were able to demonstrate that menopause causes cardiomyopathic changes, and we propose that these changes could be mediated by oxidative stress.

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