ArticleThe Journal of surgical research2013
Cellular basis of burn-induced cardiac dysfunction and prevention by mesenteric lymph duct ligation.
Article in The Journal of surgical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Hypermetabolism and Lipid Alterations Postburn: A Cardiovascular Perspective.Cardiovascular therapeutics · 2026Review
- Mesenteric Lymph Duct Ligation Alleviates Acute Lung Injury Caused by Severe Acute Pancreatitis Through Inhibition of High Mobility Group Box 1-Induced Inflammation in Rats.Digestive diseases and sciences · 2021Article
- Cardiovascular Dysfunction Following Burn Injury: What We Have Learned from Rat and Mouse Models.International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMyocardial contractile depression develops 4 to 24 h after major burn injury. We have reported previously that in a rat burn injury model (≈40% of total body surface area burn), mesenteric lymph duct ligation (LDL) prior to burn prevented myocardial dysfunction. However, the underlying cellular and molecular mechanisms are not well understood. MATERIALS AND
methodsLeft ventricular myocytes were isolated from sham burn (control), sham burn with LDL (sham + LDL), burn, and burn with LDL (burn + LDL) rats at 4 and 24 h after burn or sham burn. Electrophysiological techniques were used to study myocyte size, contractility and L-type Ca2+ channel current (ICa). Further studies examined changes in the messenger RNA expression levels of pore-forming subunit of the L-type Ca(2+) channel, α1C, and its auxiliary subunits, β1, β2, β3, and α2δ1, which modulate the abundance of the ICa in post-burn hearts.
resultsDepressed myocyte contractility (≈20%) developed during 4 to 24 h post-burn compared with control, sham + LDL, or burn + LDL groups, a pattern of changes consistent with whole heart studies. There was no significant alteration in myocyte size. The ICa density was significantly decreased (≈30%) at 24 h post-burn, whereas the messenger RNA expression levels of Ca(2+) channel gene were not significantly altered at 4 and 24 h after burn injury.
conclusionsThese results suggest that the post-burn contractile phenotype in vivo was also present in isolated myocytes in vitro, but cellular remodeling was not a major factor. The results also suggest that changes in ICa regulation, but not from Ca(2+) channel gene modification, may be a key element involved in post-burn contractile depression and the beneficial effects of LDL.
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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.