Abstract 555: Heme-Oxygenase 1 Upregulation Attenuates Acute Myocardial Reperfusion Injury and Left Ventricular Remodeling in Rats
Bibliographic record
Abstract
Background: Reperfusion injury occurring after reestablishment of blood flow after MI is thought to be mediated by reactive oxygen species and neutrophilic cellular damage. The Heme-Oxygenase-1 (HO-1) dependent decrease in oxidative stress may attenuate injury in part by inhibiting transcription factor NFκB-mediated inflammation. We tested the hypothesis that exogenous upregulation of HO-1 by hemin administration confers acute and chronic cardioprotection against I/R injury in rats and attenuates LV remodeling post-infarction. Methods: Six week-old male Wistar rats were randomly assigned to sham, vehicle, or hemin-treated groups. Vehicle and hemin were administered i.p. once daily for 3 days prior to LAD occlusion, and 48 hours post-operatively once every 3 days. Infarct size was determined by H&E histological analysis and fibrosis was quantified by Masson’s Trichrome staining. We used transthoracic echocardiography to assess LV size, function and wall motion. Results: Hemin increased HO-1 expression and decreased infarct size and fibrosis, and attenuated LV wall thinning and chamber dilatation in the short-term (4 days post-infarction). The decrease in infarct size and fibrosis in the hemin group was accompanied by a decrease in NF-κB activity. We observed no significant difference in infarct size and area of fibrosis between hemin and vehicle-treated groups at 3 months (p=0.6681, p=0.6382, respectively). Cavity dilatation did not differ between the two groups at 3 months, however attenuated interventricular septum thinning (p<0.05) was observed in the hemin group compared with the vehicle group. Conclusion: HO-1 upregulation by hemin confers acute cardioprotection and decreased inflammation, possibly by inhibiting NF-κB activity, although chronic treatment with hemin does not prevent long-term LV remodeling post-MI. Future research should focus on optimal HO-1 upregulation to attenuate long-term LV remodeling due to reperfusion injury. Left Ventricle Wall and Chamber Dimensions
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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) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 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) | 0.005 | 0.001 |
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".