ArticleBMC cardiovascular disorders2024
Comparison of heart rate variability, hemodynamic, metabolic and inflammatory parameters in various phases of decompansatory hemorrhagic shock of normal and vagotomized conscious male rats.
Article in BMC cardiovascular disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHeart rate variability (HRV) analysis has shown promise as a valuable complementary tool for clinical assessment in trauma cases. This study aims to evaluate the utility of HRV in monitoring different severities of hemorrhagic shock (HS) and its correlation with traditional hemodynamic and metabolic parameters.
methodsMale Sprague-Dawley rats were divided into different experimental groups, including those with and without vagotomy, and were exposed to different classes of decompensatory HS. To induce varying severities of HS, volume resuscitation was delayed by gradually returning 0%, 20%, or 50% of the shed blood volume at the end of the compensation phase, referred to as 0% DFR, 20% DFR, and 50% DFR class, respectively. Hemodynamic parameters were monitored, and HRV was calculated. Levels of TNF-α and IL-10 were determined in lung tissue at the end of the experiments. Correlations between HRV, hemodynamic parameters, inflammatory gene expression and arterial blood gas variables were evaluated.
resultsHRV showed increased power of the low-frequency (LF) and respiratory sinus arrhythmia (RSA) in all groups during the hypotension phase of HS (Nadir 1). Subdiaphragmatic vagotomy blunted the increase in the LF component in the Nadir 1. After volume resuscitation, systolic blood pressure (SBP), RSA and LF returned to baseline in the 0% DFR and 20% DFR classes. However, animals in 50% DFR class exhibited a reduced SBP and LF and lower pH. Notably, strong correlations were found between LF and SBP as well as tissue hypoperfusion markers. The expression of TNF-α in the lung was increased in all HS groups, while this gene expression was significantly higher in the vagotomized animals.
conclusionThe alterations in HRV components were found to be significantly correlated with the hemodynamic and metabolic status of the animals, while showing no association with inflammatory responses. Additionally, the intervention of subdiaphragmatic vagotomy significantly impacted both HRV components and inflammatory responses. Collectively, these findings suggest the potential of HRV components for the assessment of the presence and severity of HS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.