Why the study?
Sepsis-induced myocardial injury is considered not to involve leukocyte infiltration into myocytes, prompting investigation into neutrophil recruitment crosstalk in its pathogenesis.
Sepsis induces significant myocardial injury, inflammation, and apoptosis in a mouse model, highlighting the role of inflammatory mediators in sepsis-induced cardiomyopathy.
Animal CLP model data on sepsis myocardial crosstalk mechanisms are hypothesis-generating; leaves open human translation.
Acute myocardial injury may be induced by different causes, including myocardial ischemia-reperfusion injury, and sepsis, which represent the most common reasons for cardiac injury in hospitalized patients. Sepsis-induced myocardial injury is considered not to be associated with leukocyte infiltration into the myocytes but is shared with many crosstalk pathogeneses. In this experimental animal study, polymicrobial sepsis-induced was via cecal ligation and puncture model (CLP), in C57BL/6 male mice (25–30 g). By using neutrophil knockout mice, in which neutrophil recruitment is impaired, we analyzed the specific contribution to the pathogenesis of CLP-induced attenuated myocardial function. We investigated the degree of myocardial injury evaluated by plasma troponin, echocardiography, and histological analyses. The pathogenesis of CLP-induced myocardial injury relies on circulating inflammatory mediators. In conclusion, these resulting data explained that myocardial injury pathogenesis may help in the treatments for myocardial injury patients.
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Sarfaraz et al. (2023) studied this question.
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