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Antioxidant and oxidative stress changes in experimental cor pulmonale
Firoozeh Farahmand1, Michael F Hill, Pawan K Singal
1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Canada.
Molecular and Cellular Biochemistry
|July 2, 2004
Summary
Right heart failure (RHF) involves oxidative stress, with antioxidant enzymes increasing during hypertrophy and decreasing during failure. This suggests oxidative stress plays a key role in RHF development.
Area of Science:
- Cardiovascular Research
- Pathophysiology
- Biochemistry
Background:
- Right heart failure (RHF) is a significant cardiovascular complication, often understudied compared to left heart failure.
- Oxidative stress and antioxidant mechanisms are implicated in the progression from cardiac hypertrophy to failure.
Purpose of the Study:
- To investigate the role of antioxidants and oxidative stress in the progression of right ventricular hypertrophy to failure.
- To characterize the temporal changes in oxidative stress markers during the development of RHF induced by monocrotaline (MCT).
Main Methods:
- Right heart failure was induced in rats using a single injection of monocrotaline (MCT).
- Animals were assessed at 1, 2, and 6 weeks post-injection, evaluating hemodynamic, clinical, and histopathological parameters.
- Changes in antioxidant enzyme activities and lipid peroxidation were measured.
Main Results:
- Early stages (1-2 weeks) showed right ventricular (RV) hypertrophy, increased antioxidant enzymes, and preserved function.
- Later stage (6 weeks) exhibited overt RHF with RV dilation, decreased antioxidant enzyme activity, and increased lipid peroxidation.
- Significant changes in interventricular septum (IVS) morphology were observed, bulging into the left ventricle (LV).
Conclusions:
- MCT-induced pulmonary hypertension leads to biphasic changes in RV antioxidant enzymes.
- An increase in antioxidants during hypertrophy suggests a compensatory mechanism.
- A decrease in antioxidants during RHF indicates a potential role for oxidative stress in RV dysfunction pathogenesis.