ArticleResuscitation plus2025
Temporal profiling of myocardial inflammation and recovery in a murine model of cardiac arrest and adrenaline exposure.
Article in Resuscitation plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Systemic inflammatory response drives post-cardiac arrest multi-organ injury via IL-17 signaling in murine and porcine models.Frontiers in immunology · 2026Article
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Authors and funding
7 authors.
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Abstract
Background: Myocardial dysfunction after cardiac arrest (CA) is a major contributor to poor outcomes, yet the underlying inflammatory mechanisms within cardiac tissue remain incompletely defined. We sought to delineate the temporal evolution of myocardial inflammation following CA, distinguishing the effects of ischemia-reperfusion injury from those of adrenaline exposure alone. Methods and Results: Using a murine model of CA and resuscitation, we profiled transcriptomic, immunologic, and functional cardiac changes in mice exposed to either CA followed by resuscitation with adrenaline (Arrest group), adrenaline alone (Adr group), or anesthesia alone (Naïve group). Animals were assessed at 0.5-, 1-, 3-, and 7-days via echocardiography, RNA-sequencing, flow cytometry, immunohistochemistry, and multiplex cytokine analysis. CA elicited a robust, early myocardial inflammatory response characterized by neutrophil infiltration, systemic cytokine surges (IL-6, TNF-α, IL-1β), and downregulation of mitochondrial and metabolic pathways. This immune activation peaked at 0.5 days and resolved by day 7, coinciding with transient myocardial dysfunction and recovery of ejection fraction. In contrast, adrenaline alone induced a delayed, attenuated response peaking at 1 day. Transcriptomic and immunophenotypic signatures distinguished ischemia-driven injury from catecholaminergic effects. Conclusions: CA induces a distinct, self-limited myocardial inflammatory cascade that parallels functional cardiac recovery. These findings identify a narrow therapeutic window for immunomodulatory interventions and provide a mechanistic foundation for targeted therapies to mitigate cardiac injury after resuscitation.
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Registered trials
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