Role of nitric oxide in mediating cardiovascular alterations accompanying heart failure in rats
Bibliographic record
Abstract
The present study was designed to evaluate the role of endothelial NO in the hemodynamics and vascular changes that occur in heart failure following myocardial infarction in rats. Left ventricular systolic pressure (LVSP), mean blood pressure (MBP), aortic morphology (media thickness) and reactivity were evaluated in rats with coronary artery ligation (heart failure, HF) or sham operation (SO) untreated or treated for four weeks with either a low dose of NG-nitro-L-arginine methyl ester (L-NAME, 6 mg.kg(-1).day(-1)) or L-arginine (1.5 g.kg(-1).day(-1)). In rats with HF LVSP (HF = 111 +/- 8 mmHg; SO = 143 +/- 6 mmHg, p < 0.05), MBP (HF = 98 +/- 8 mmHg; SO = 127 +/- 6 mmHg, p < 0.05) and aortic media thickness (HF = 68 +/- 6 microm; SO = 75 +/- 2 microm, p < 0.05) were significantly reduced. The contractile response to phenylephrine and the endothelium-independent relaxation to sodium nitroprusside were similar in HF and SO aortas, but the sensitivity (pD2) to acetylcholine (HF = 7.5 +/- 0.06; SO = 7.1 +/- 0.08, p < 0.05) was significantly increased in HF aortas, indicating an enhanced basal NO release. Treatment with L-NAME (LN) reversed the effects of HF on LVSP (HF-LN = 143 +/- 9 mmHg, p < 0.05 vs. HF), MBP (HF-LN = 128 +/- 8 mmHg, p < 0.05 vs. HF), sensitivity to acetylcholine (HF-LN = 6.9 +/- 0.10, p < 0.05 vs. HF) and aortic media thickness (HF-LN = 79 +/- 2 microm, p < 0.05 vs. HF), without changing these parameters in SO rats. L-NAME also selectively increased the maximal response to phenylephrine in HF aortas (HF-LN = 2.4 +/- 0.20 g; HF = 1.6 +/- 0.17 g, p < 0.05). L-arginine (LA) did not change the effects of HF on LSVP, MBP or aortic media thickness, but it reduced the sensitivity to phenylephrine in aortas from SO rats (SO-LA = 6.5 +/- 0.12; SO = 7.0 +/- 0.09, p < 0.05). Taken together, these results suggest an important role for endothelial NO in mediating the reduced vascular growth, myocardial dysfunction and hypotension in rats with HF.
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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".