It is well known that cardiac dysfunction in sepsis is associated with significantly increased mortality. The pathophysiology of sepsis-induced cardiac dysfunction can be summarized as involving impaired myocardial circulation, direct myocardial depression, and mitochondrial dysfunction. Impaired blood flow to the myocardium is associated with microvascular dysfunction, impaired endothelium, and ventriculo-arterial uncoupling. The mechanisms behind direct myocardial depression consist of downregulation of β-adrenoceptors and several myocardial suppressants (such as cytokine and nitric oxide). Recent research has highlighted that mitochondrial dysfunction, which results in energy depletion, is a major factor in sepsis-induced cardiac dysfunction. Therefore, the authors summarize the pathophysiological process of cardiac dysfunction in sepsis based on the results of recent studies.

Extracorporeal membrane oxygenation (ECMO) use has remarkably increased in recent years. Although ECMO has become essential for patients with refractory cardiac and respiratory failure, extracorporeal circulation (ECC) is associated with significant complications. Small-animal models of ECC have been developed and widely used to better understand ECC-induced pathophysiology. This review article summarizes the development of small-animal ECC models, including the animal species, circuit configuration, priming, perioperative procedures, cannulation, and future perspectives of small-animal ECMO models.

Acute myocardial infarction is the most common form of coronary artery disease, and myocardial ischemia–reperfusion injury remains a major challenge despite advances in reperfusion therapy. Endotoxin preconditioning has been linked to reduced ischemia–reperfusion injury, but mechanisms remain unclear, and prior studies have used varied assessment methods with inconsistent results. In this study, we confirmed the protective effect of endotoxin preconditioning and assessed its role in preserving mitochondrial respiration using a multi-model approach of in vivo ischemia–reperfusion rat model, ex vivo normothermic rat heart perfusion, and in vitro hypoxia–reoxygenation in neonatal rat cardiomyocytes. Hemodynamic and cell-based analyses were performed in control (n = 5), ischemia–reperfusion/hypoxia–reoxygenation (n = 4/3), and endotoxin-pretreated (n = 5/3) groups. Low-dose endotoxin pretreatment significantly preserved left ventricular function, myocardial oxygen consumption, and mitochondrial respiration (p < 0.001). Preservation of function was associated with reduced hypoxia-inducible factor 1-alpha (HIF-1α) expression and decreased mitochondrial superoxide production, indicating reduced oxidative stress. Nonlethal endotoxin pretreatment protects the myocardium from ischemia–reperfusion injury by sustaining mitochondrial respiration and limiting oxidative damage. These findings support further investigation in large animal models to better replicate human myocardial infarction and evaluate translational potential.

Purpose: The objective of this study was to evaluate the effect of Polymyxin B hemoperfusion (PMX-HP) on patients with sepsis.Methods: A systematic review and meta-analysis was performed using relevant articles retrieved from 3 databases (PubMed, Cochrane Library, EMBASE). Randomized studies from 1 January 1999 to 28 February 2022 were examined to determine the clinical results of PMX-HP. A meta-analysis was carried out using the random-effects method, meta-regression with clinical variables, and assessment of risk of bias (ROB) tool (Cochrane ROB assessment tool). Mortality was evaluated within 60 days of hospitalization (in-hospital death 28-day, 30-day, and 60-day mortality) and predictors associated with mortality were determined using meta-regression.Results: There were 11 randomized studies with 548 patients included in the meta-analysis. The pooled mortality was 35% (95% CI, 27%-42%, 95% CI 0.53-0.96). Further subgroup analysis was performed according to the duration of PMX-HP. An extension of PMX-HP treatment beyond 2 hours (pooled mortality, 43%; 95% CI, 9%-76%) compared with a 2-hour session (pooled mortality, 33%. 95% CI, 27%-38%) showed an increase in mortality rates. However, this was not statistically significant. Univariate meta-regression showed that patient’s age, the acute physiology and chronic health evaluation score, and the sequential organ failure assessment score did not significantly impact mortality.Conclusion: While PMX-HP is valuable in the management of septic shock, treatment duration should be based on careful assessment of the patient's condition, the risks and benefits of prolonged therapy, and the overall treatment strategy including antimicrobial management and source control.

Background and Objectives: Normothermic ex situ heart preservation maintains donor heart viability by sustaining physiological conditions and reducing ischemic damage. However, the ideal perfusion pressure remains uncertain. This study aims to identify the optimal perfusion pressure to enhance graft preservation in rat heart transplantation. Materials and Methods: We utilized 20 male Sprague-Dawley rats (400–500 g). Donor hearts underwent normothermic preservation for 2 h using a Langendorff apparatus primed with 12 mL of solution at a consistent 3 mL/min flow. After preservation, hearts were transplanted heterotopically into the recipient’s abdomen. We defined successful preservation by observing a QRS complex in electrocardiographic monitoring for 3 h post-transplantation. Histological assessments for myocardial integrity occurred after 4 h of reperfusion. We analyzed statistical differences between successful and unsuccessful preservation groups. Results: Electrocardiograms indicated preservation failure in 8 of the 20 donor hearts due to the absence of a QRS complex. We observed no significant differences in ischemic duration between groups. At 120 min, although serum lactate and potassium concentrations increased in the unsuccessful group, the differences were not statistically significant. Higher initial perfusion pressures (>65 mmHg) at a constant flow rate resulted in elevated lactate and potassium concentrations post-preservation, indicating suboptimal outcomes. Histologically, hematoxylin and eosin staining showed better myocardial preservation in successful hearts, while TUNEL assays demonstrated increased apoptosis in unsuccessful hearts. All hearts increased in weight after preservation, but significant increases occurred only in unsuccessful cases. Conclusions: Higher initial perfusion pressures (>65 mmHg) negatively affect heart preservation outcomes, resulting in elevated serum lactate and potassium levels, increased heart weight, and greater histological damage. Maintaining optimal perfusion pressures is essential to preserve myocardial integrity and functional viability during normothermic ex situ heart preservation.