Background: Sepsis-induced myocardial injury is one of the major predictors of morbidity and mortality of sepsis. The cytoprotective function of erythropoietin (EPO) has been discovered and extensively studied. However, the cardioprotective effects of EPO on sepsis-induced myocardial injury in the rat sepsis model has not been reported.
Methods: The rat models of sepsis were produced by cecal ligation and perforation (CLP) surgery. Rats were randomly (random number) assigned to one of three groups (n=8 for each group): sham group, CLP group and EPO group (1000 IU/kg erythropoietin). Arterial blood was withdrawn at 3, 6, 12, and 24 hours after CLP. cTnI, BNP, CK-MB, LDH, AST, TNF-α, IL-6, IL-10, and CRP were tested by the ELISA assay. Changes of hemodynamic parameters were recorded at 3, 6, 12, 24 hours after the surgery. Histological diagnosis was made by hematoxylin and eosin. Flow cytometry was performed to examine cell apoptosis, myocardium mitochondrial inner membrane potential, and NF-κB (p65). Survival rate at 7 days after CLP was recorded.
Results: In the CLP group, myocardial enzyme index and inflammatory index increased at 3, 6, 12 and 24 hours after CLP compared with the sham group, and EPO significantly blocked the increase. Compared with the CLP group, EPO significantly improved LVSP, LV +dp/dt max, LV -dp/dt min, and decreased LVEDP at different time. EPO blocked the reduction of mitochondrial transmembrane potential, suppressed the cardiomyocyte apoptosis, inhibited the activation of NF-κB, and reduced the production of proinflmmatory cytokines. No difference in the survival rate at 7 days was observed between the CLP group and the EPO group.
Conclusion: Exogenous EPO has cardioprotective effects on sepsis-induced myocardial injury.
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http://dx.doi.org/10.5847/wjem.j.issn.1920-8642.2013.03.011 | DOI Listing |
Cureus
December 2024
Internal Medicine, Kempegowda Institute of Medical Sciences, Bangalore, IND.
Sepsis-induced cardiomyopathy (SICM) is a life-threatening complication of sepsis characterized by myocardial dysfunction. SICM significantly increases mortality rates in sepsis. Despite its clinical relevance, SICM lacks a unified definition and standardized diagnostic criteria, complicating early identification and treatment.
View Article and Find Full Text PDFJ Cardiothorac Surg
January 2025
Emergency and Critical Care Center, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
Purpose: We sought to investigate the expression of MALAT1, plasma brain natriuretic peptide, and Tei index in sepsis-induced myocardial injury.
Methods: The current retrospective analysis focused on 146 sepsis patients admitted to our hospital from February 2021 to March 2023. Based on the presence or absence of myocardial injury, the patients were divided into two groups: the sepsis group (n = 80) and the sepsis-induced myocardial injury group (n = 66).
J Intensive Care
January 2025
Department of Medicine, John A. Burns School of Medicine, University of Hawai'i, Honolulu, HI, USA.
Sepsis often leads to vasoplegia and a hyperdynamic cardiac state, with treatment focused on restoring vascular tone. However, sepsis can also cause reversible myocardial dysfunction, particularly in the elderly with pre-existing heart conditions. The Surviving Sepsis Campaign Guidelines recommend using dobutamine with norepinephrine or epinephrine alone for patients with septic shock with cardiac dysfunction and persistent hypoperfusion despite adequate fluid resuscitation and stable blood pressure.
View Article and Find Full Text PDFRedox Rep
December 2025
Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, People's Republic of China.
Objective: Inflammation and oxidative damage play critical roles in the pathogenesis of sepsis-induced cardiac dysfunction. Multiple EGF-like domains 9 (MEGF9) is essential for cell homeostasis; however, its role and mechanism in sepsis-induced cardiac injury and impairment remain unclear.
Methods: Adenoviral and adeno-associated viral vectors were applied to overexpress or knock down the expression of MEGF9 in vivo and in vitro.
World J Cardiol
December 2024
Clinical College of Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China.
The maintenance of intracellular and extracellular adenosine triphosphate (ATP) levels plays a pivotal role in cardiac function. In recent years, burgeoning attention has been directed towards ATP-induced cell death (AICD), revealing it as a distinct cellular demise pathway triggered by heightened extracellular ATP concentrations, distinguishing it from other forms of cell death such as apoptosis and necrosis. AICD is increasingly acknowledged as a critical mechanism mediating the pathogenesis and progression of various cardiovascular maladies, encompassing myocardial ischemia-reperfusion injury, sepsis-induced cardiomyopathy, hypertrophic cardiomyopathy, arrhythmia, and diabetic cardiomyopathy.
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