Modulation of oxidative stress and antioxidants by losartan in heart failure
Bibliographic record
Abstract
In patients surviving a myocardial infarction M), the heart undergoes a remodefing process characterized by hypertrophy which can also lead to heart failure. Although hypertrophy is an early response that may temporarily preserve cardiac function, numerous studies have suggested that this long term process of remodefing is also associated with an increase in oxidative stress and cardiac decompensation. The objectives of the present research on rat hearts subsequent to MI therefore, were to: (i) characterize changes in the oxidative stress and enzymatic antioxidants, (superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and catalase) in relation to their rnRNA abundance and protein content; (ii) study changes in nonenzymatic antioxidants at different stages of heart failure in relation to cardiac function in order to have a more comprehensive information about the antioxidant reserve, and (iii) study the effects of RAS inhibition at the AT1 receptor site by losartan on the myocardial enzymatic and non-enzymatic antioxidants (SOD, GSHPx, catalase, vitamins A and E) and oxidative stress (Lipid hydroperoxides, reduced and oxidized glutathione and the redox ratio) in relation to the changes in hemodynamic function during the sequelae of congestive heart failure. It is concluded that inhibition of the RAS at the AT1 receptor site with losartan, in addition to reducing cardiac remodeling and improving hemodynamic function, reduces oxidative stress and improves myocardial endogenous antioxidants subsequent to myocardial infarction. The study suggests a newer role for losartan in the treatment of heart failure. Although changes in the SOD and catalase activities during heart failure correlated with changes in mRNA for these enzymes, the precise mechanism/s for decrease in oxidative, stress and improvement in antioxidant reserve after losartan treatment is/are unclear at this time. (Abstract shortened by UMI.)
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".