Anakinra and Myocardial Injury After Cardiac Arrest in Rats

INTRODUCTION: Objective: 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 effects of anakinra on early myocardial histopathological changes in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary resuscitation.
METHODS: Materials and Methods: 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.
RESULTS: Results: 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 in any group.
DISCUSSION AND CONCLUSION: Conclusion: 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.

Keywords: Anakinra, cardiac arrest, cardiopulmonary resuscitation, interleukin-1, myocardial injury, rat.