Key result
Mild acidosis reduces cardiac contractility and impairs the beta-adrenergic response to isoproterenol in isolated human failing myocardium compared to pH 7.40.
Why the study?
Does mild acidosis (pH 7.20) reduce cardiac contractility in isolated human failing myocardium compared to normal pH (7.40)?
Does mild acidosis (pH 7.20) reduce cardiac contractility in isolated human failing myocardium compared to normal pH (7.40)?
Answers are grounded in this paper and cite their sources.
This commentary highlights ex vivo data confirming that mild acidosis directly impairs contractility in human failing myocardium, emphasizing the clinical importance of managing acidosis in shock states.
Acidosis is one of the major consequences of hemodynamic instability in shock state patients directly associated with multiple organ failure evolution and death. Most studies on the hemodynamic consequences of acidosis have been experimental, nonhuman studies with severe acidosis, and thus far from the most common clinical situations. Schotola and colleagues offer a new approach to human failing myocardium where the authors highlight, ex vivo, the deleterious hemodynamic consequences of mild acidosis. Their work strengthens the current view of the urgent need to discover new efficient and nondeleterious therapy for the treatment of acidosis.
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Kimmoun et al. (2012) conducted an editorial in Acidosis in shock state / failing myocardium. Mild acidosis (pH 7.20) vs. Normal pH (7.40) was evaluated on Cardiac contractility in response to isoproterenol. Mild acidosis reduces cardiac contractility and impairs the beta-adrenergic response to isoproterenol in isolated human failing myocardium compared to pH 7.40.
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