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Higher antioxidative capacity during a chronic stable heart hypertrophy
1Cardiovascular Sciences Division, St. Boniface General Hospital Research Center, Winnipeg, Canada.
Insights
Chronic pressure overload in rats leads to stable heart hypertrophy with increased antioxidative capacity. This enhanced defense mechanism protects the heart from oxygen radical damage, maintaining function during sustained overload.
Area of Science:
- Cardiovascular Physiology
- Biochemistry
- Oxidative Stress Research
Background:
- Heart hypertrophy, a thickening of the heart muscle, can result from chronic pressure overload.
- Understanding the biochemical adaptations, particularly concerning oxygen radicals, is crucial for managing cardiac function during sustained stress.
Purpose of the Study:
- To investigate the changes in oxygen radical mechanisms in rat hearts during the development of stable hypertrophy over 6-48 weeks.
- To assess the antioxidative capacity and its role in maintaining cardiac function under chronic pressure overload.
Main Methods:
- Induction of heart hypertrophy via subdiaphragmatic aortic banding in rats.
- Measurement of cardiac function parameters (left ventricular pressure, dP/dt).
- Assay of antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase) and lipid peroxidation (malondialdehyde).
- Ex vivo perfusion of hearts with xanthine-xanthine oxidase to assess radical-induced damage.
Main Results:
- Hypertrophied hearts exhibited stable hyperfunction without signs of heart failure.
- Superoxide dismutase activity was elevated early in hypertrophy, while glutathione peroxidase remained elevated throughout.
- Lipid peroxide levels were lower in hypertrophied hearts.
- Hypertrophied hearts showed better resistance to contractile dysfunction induced by exogenous oxygen radicals.
Conclusions:
- Stable heart hypertrophy under chronic pressure overload is associated with an increased antioxidative capacity.
- Enhanced antioxidant defense mechanisms contribute to the maintenance of cardiac function during sustained pressure overload.
- These findings suggest a protective adaptation in the hypertrophied heart against oxidative stress.
Abstract:
Changes in oxygen radical mechanisms during 6-48 weeks of heart hypertrophy in rats subjected to a narrowing of the subdiaphragmatic aorta were examined. During this period, hypertrophied hearts demonstrated a stable hyperfunction, as indicated by an elevated but stable left ventricular systolic pressure, dP/dt, and aortic pressure and no change in left ventricular end diastolic pressure. Experimental animals showed increased heart-to-body weight ratios; however, the conventional signs of heart failure such as increased wet-to-dry weight ratios of liver and lung, ascites, or pleural effusion were absent. Hearts were examined for superoxide dismutase, glutathione peroxidase, and lipid peroxide activities. The superoxide dismutase activity was significantly higher in hypertrophied hearts at 6 and 12 weeks as compared with sham-operated rats (sham controls), while no difference was seen at 24 and 48 weeks due to a marked increase in the superoxide dismutase activity of sham control hearts in these age groups. During the period studied, glutathione peroxidase activity remained unchanged in controls but was significantly elevated in hypertrophied hearts. Lipid peroxide activity as indicated by the malondialdehyde content was significantly lower in hypertrophied hearts. Perfusion of isolated control and hypertrophy hearts with xanthine-xanthine oxidase, an exogenous source of oxygen radicals, resulted in contractile failure and rise in resting tension. In hypertrophied hearts, however, the contractile force was better maintained and there was a lesser rise in resting tension after exposure to xanthine-xanthine oxidase. The study suggests the development of a higher antioxidative capacity during the stable phase of hypertrophy due to a chronic pressure overload.