AMP-activated protein kinase protects against sepsis-induced left ventricular wall edema by preserving interendothelial tight junctions, which may have implications for diastolic dysfunction in sepsis patients.
Hypothesis-generating for AMPK in sepsis-induced LV edema; should not yet change clinical practice.
Our results demonstrate for the first time the involvement of a signaling pathway in the control of left ventricular wall edema during sepsis. AMP-activated protein kinase exerts a protective action through the preservation of interendothelial tight junctions. Interestingly, exaggerated left ventricular wall edema was not coupled with aggravated systolic dysfunction. However, it could contribute to diastolic dysfunction in patients with sepsis.
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Castanares‐Zapatero et al. (2013) studied this question.
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