CHEST Guidelines-Adrenergic-Overstimulation

Adrenergic-Overstimulation_chest

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In a recent issue of CHEST, a correspondence by Daniele Orso and Roberto Copetti addresses the topic of adrenergic overstimulation as a contributing factor in sepsis-related cardiomyopathy, a point they felt was not sufficiently covered in an earlier paper by Martin et al. The authors argue that continuous adrenergic stimulation, through the activation of beta-1 receptors, can lead to cardiac dysfunction by initiating apoptotic pathways via increased intracellular calcium influx and downregulation of beta receptors. These processes may be exacerbated by molecules like inducible nitric oxide, often stimulated by endotoxins from gram-negative bacteria.<br /><br />Orso and Copetti suggest that exploring this hypothesis is crucial for advancing understanding of the damage mechanisms not only in sepsis but also in syndromes like burns and trauma. Moreover, confirming this model through clinical trials could elucidate reasons for the non-efficacy of catecholamines in certain septic patients, potentially paving the way for alternative treatments, such as beta-blockers, which preliminary studies suggest may improve survival rates.<br /><br />In response, Martin et al. acknowledge adrenergic overstimulation as a notable factor in septic cardiomyopathy, highlighting it as a potentially debatable contributor within the condition's pathophysiology. They discuss the therapeutic potential of modulating b1 and b2-adrenergic receptor signaling to mitigate inflammation in sepsis-affected hearts. However, they note the lack of established efficacy for beta-adrenergic blockade therapy in septic shock, despite some positive findings from initial studies.<br /><br />The dialogue underscores ongoing exploration and contentions surrounding adrenergic mechanisms in sepsis, signifying an area ripe for further research to potentially develop targeted therapeutic strategies.

Keywords

adrenergic overstimulation

sepsis-related cardiomyopathy

beta-1 receptors

cardiac dysfunction

intracellular calcium influx

inducible nitric oxide

catecholamines

beta-blockers

septic shock

therapeutic strategies