Alterations to Venular Function in Skeletal Muscle with Metabolic Syndrome
Bibliographic record
Abstract
While the overwhelming majority of research into vascular outcomes of the metabolic syndrome have focused on the arterial/arteriolar and capillary levels, investigation into venular function and how development of metabolic syndrome impacts responses has received little attention. Using the in situ cremaster muscle of obese Zucker rats (OZR) as compared to control leans (LZR), we determined indices of venular network structure as well as vessel structure and function. At ~17 weeks of age, skeletal muscle post‐capillary venular density was reduced by ~20% in LZR vs. OZR, although there was no evidence of remodeling of the wall of individual venules impacting passive diameter. Initial basal diameter and blood flow within individual venules of ~25 mm and ~ 60 mm diameter was similar between LZR and OZR, although an increased variability was evident. Dilator responses to acetylcholine were consistently blunted in venules of OZR vs. LZR, and this reflected multiple effects: including an oxidant stress‐based loss of venular nitric oxide bioavailability, an increased constrictor tone from TxA 2 and an increased constrictor tone mediated via the α 1 adrenergic receptor. Impaired dilator responses were also coupled to vessels where increased leukocyte adhesion/rolling was clearly present. Venular constrictor responses between LZR and OZR were comparable for angiotensin II, endothelin and α 2 adrenoreceptor stimulation, although responses to α 1 adrenoreceptor stimulation were mildly elevated, but with increased variability. In response to field stimulation of the cremaster muscle (0.5 or 1/s, 400 ms duration, 60 Hz within train, 7V), venular dilator and hyperemic responses to contraction were blunted in OZR vs. LZR, but responses at the higher frequency were similar in magnitude. These results suggest that alterations in venular function may contribute to dysregulation of flow distribution in skeletal muscle with metabolic syndrome and impair parameters of mass transport and exchange. Support or Funding Information National Institutes of Health; American Heart Association
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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 | 0.001 | 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 | 0.000 |
| 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".