Cardiac neuromodulation with acute intermittent hypoxia in rats with spinal cord injury
Bibliographic record
Abstract
It is well recognized that the interruption in bulbospinal sympathetic projections is the main cause of cardiovascular instability in individuals and experimental animals with spinal cord injury (SCI). Whether interrupted bulbospinal sympathetic projections contribute to cardiac dysfunction directly (i.e. input to the heart) or indirectly (i.e. vascular influences that alter loading conditions on the heart) post-SCI remains unknown, as does the potential effect of SCI-induced alterations in parasympathetic control on heart function. We employed a sequential pharmacological blockade approach to bridge this knowledge gap and additionally examined whether acute intermittent hypoxia (AIH) is capable of neuromodulating the heart post-SCI. In two experiments, rats were given T3 contusion SCI and survived for 2 weeks. At 2 weeks post-SCI, rats were instrumented with left ventricular and arterial catheters to assess cardiovascular function in response to either a sequential pharmacological blockade targeting different sites of the autonomic neuraxis (experiment 1) or AIH (experiment 2). The findings from experiment 1 revealed that impaired direct sympathetic transmission to the heart underlies the majority of the SCI-induced reduction in heart function post-SCI. The findings from experiment 2 revealed that a single-session of AIH increased left ventricular pressure generation and arterial blood pressure immediately and up to 90 min post-AIH. Together, our findings demonstrate that disrupted bulbospinal sympathetic pathways contribute directly to the SCI-induced impairment in left ventricular function. We also show that a single session of AIH is capable of neuromodulating the heart post-SCI. KEY POINTS: The loss of sympathetic transmission to the heart is the main cause of reduced cardiac function in a rodent model of spinal cord injury (SCI). Parasympathetic control remains unaltered post-SCI and does not contribute to reduced cardiac function post-SCI. Acute intermittent hypoxia neuromodulates the heart and increases left ventricular pressure generating capacity.
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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 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 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".