Key result
Anakinra lowers early post-resuscitation myocardial congestion scores by ~1 point vs. sham after cardiac arrest.
Why the study?
Interleukin-1 blockade may modulate ischemia-reperfusion injury, but the histopathological effects of anakinra on myocardial tissue early after cardiac arrest and cardiopulmonary resuscitation remain unclear.
Does intraperitoneal anakinra reduce early myocardial histopathological changes (fiber disorganization, interstitial edema, congestion, and leukocyte infiltration) in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary resuscitation?
Does intraperitoneal anakinra reduce early myocardial histopathological changes (fiber disorganization, interstitial edema, congestion, and leukocyte infiltration) in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary resuscitation?
In a rat model of asphyxia-induced cardiac arrest and resuscitation, interleukin-1 blockade with anakinra selectively attenuated early myocardial microvascular congestion without significantly improving myocardial fiber disorganization or interstitial edema.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in rat cardiac arrest model; leaves open translation to human post-arrest care.
Post-cardiac arrest myocardial injury is an important component of post -cardiac arrest syndrome and is associated with global ischemia-reperfusion, endothelial dysfunction, oxidative stress, and inflammatory activation.Interleukin -1 blockade may modulate ischemia-reperfusion injury; however, its histopathological effects on myocardial tissue after cardiac arrest remain unclear.This study aimed to evaluate the effect s of anakinra on early myocardial histopathological changes in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary resuscitation.Twenty-four male Wistar Albino rats were randomly divided into three groups: control, sham, and anakinra groups , with eight rats in each group.Cardiac arrest and cardiopulmonary resuscitation were performed in the sham and anakinra groups.After resuscitation, the sham group received intraperitoneal 0.9% NaCl, whereas the anakinra group received intraperitoneal anakinra at a dose of 50 mg/kg.Cardiac tissues were collected at the sixth minute after intervention and examined histopathologically.Myocardial fiber disorganization, interstitial edema, congestion, and polymorphonuclear leukocyte infiltration were graded semi-quantitatively.Myocardial fiber disorganization, interstitial edema, and congestion differed significantly among the groups.Compared with the sham group, anakinra significantly reduced myocardial congestion scores (p = 0.015).However, it did not significantly improve myocardial fiber disorganization or interstitial edema.Polymorphonuclear leukocyte infiltration was not observed at the early post-resuscitation time point examined in any group.Anakinra significantly attenuated myocardial congestion in the early period after asphyxia -induced cardiac arrest and resuscitation, suggesting a selective effect on the microvascular component of post -resuscitation myocardial injury.
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Ceylan et al. (2026) studied Asphyxia-induced cardiac arrest and post-resuscitation myocardial injury (n=24). Anakinra vs. Sham (0.5 mL of 0.9% NaCl intraperitoneally) and untreated Control was evaluated on Histopathological myocardial congestion score (0-3 semi-quantitative scale) at 6 minutes post-resuscitation (r = 0.61, p=0.015). Anakinra (50 mg/kg) significantly reduced early post-resuscitation myocardial congestion scores compared to sham (median 1 vs 2, p = 0.015) in rats after cardiac arrest, without improving edema.
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