ArticleActa Cardiologica Sinica2017
Surgical Acute Volume-Overload Impacts Early on Myocardium - An Experimental Study.
Article in Acta Cardiologica Sinica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- Myocardial interaction of apixaban after experimental acute volume overload.The Journal of international medical research · 2022Article
- Early reversibility of histological changes after experimental acute cardiac volume-overload.American journal of cardiovascular disease · 2022Article
- Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload.Anatolian journal of cardiology · 2019Article
- Sodium Tanshinone IIA Sulfonate Improves Hemodynamic Parameters, Cytokine Release, and Multi-Organ Damage in Endotoxemia Rabbits.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute volume-overload (AVO) predisposes to cardiac failure. Global cardiac injury may ensue after acute right-sided distension of the heart due to AVO. We experimentally investigated whether surgical AVO impacts early on the myocardium and some markers of injury.
methodsThirty-four syngeneic Fisher rats underwent surgical abdominal aortocaval fistula to induce AVO. The hearts were procured for regional and quantitative histology after one and three days. Gene expressions for atrial natriuretic peptide (ANP), matrix metalloprotease 9 (MMP9), transforming growth factor β (TGFβ) and YKL40 were investigated for myocardial injury.
resultsThe relative number of ischemic intramyocardial arteries were abundant in the septum of the hearts with AVO compared with controls at day 1 and 3 [0.16 ± 0.02 vs. 0.02 ± 0.01, point score unit (PSU), p = 0.002 and 0.14 ± 0.02 vs. 0.02 ± 0.01, PSU, p = 0.009, respectively] followed by similar changes in the left ventricle at day 3 (0.11 ± 0.02 vs. 0.04 ± 0.01, PSU, p = 0.007). Indicating early myocardial injury, ANP (p = 0.019) was increased in AVO hearts as compared with controls at day 1, as expected. More interestingly, MMP9 (p = 0.003 and p = 0.006), TGFβ (p = 0.002 and p = 0.004) and YKL40 (p = 0.001 and p = 0.003) expressions were significantly increased at day 1 and 3, along with macrophage infiltration into the myocardium supporting the role of factors produced by alternatively activated macrophages in the pathogenesis of AVO-induced pathophysiology in the heart.
conclusionsSurgical AVO induces an early ischemic myocardial response observed in the intramyocardial arteries. Early expression of key parameters of cardiac remodeling suggest for the onset of early cardiac failure after AVO.
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