Key result
In rat ventricular myocytes, 50 ng/mL TNF-α acutely reduced the amplitude of systolic intracellular calcium by 31% and systolic shortening by 19%, without affecting diastolic function.
Population
Rat ventricular myocytes
Design
Preclinical
Follow-up
acute (immediate and sustained)
Authors
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TNF-α impairs myocyte contractility via reduced SR Ca; leaves open direct role in septic cardiomyopathy and need for in vivo confirmation.
Effect estimate: 31% reduction in systolic [Ca(2+)]i and 19% reduction in systolic shortening
In rat ventricular myocytes, TNF-α acutely impairs systolic function by reducing sarcoplasmic reticulum calcium content, but does not provide a cellular mechanism for sepsis-related diastolic dysfunction.
Greensmith et al. (2013) studied Myocardial dysfunction in sepsis and septic shock. Tumor necrosis factor-alpha (TNF-α) was evaluated on Global intracellular calcium ([Ca(2+)]i), contractility, and [Ca(2+)]i handling (31% reduction in systolic [Ca(2+)]i and 19% reduction in systolic shortening). In rat ventricular myocytes, 50 ng/mL TNF-α acutely reduced the amplitude of systolic intracellular calcium by 31% and systolic shortening by 19%, without affecting diastolic function.
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