Experimental blunt chest trauma-induced myocardial inflammation and alteration of gap-junction protein connexin 43.

Miriam Kalbitz,Jochen Pressmar,Elisa Maria Amann,Martin Wepler,Belinda Bosch,Rolf Brenner,Markus Huber-Lang,Birte Weber,Hubert Schrezenmeier,Annette Palmer,Florian Gebhard,Anke Schultze,Meijing Wang

doi:10.1371/journal.pone.0187270

Miriam Kalbitz, Jochen Pressmar + Show 11 more

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https://doi.org/10.1371/journal.pone.0187270

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Abstract

ObjectiveSevere blunt chest trauma in humans is associated with high mortality rates. Whereas lung tissue damage and lung inflammation after blunt chest trauma have extensively been investigated, the traumatic and posttraumatic effects on the heart remain poorly understood. Therefore, the purpose of this study was to define cardiac injury patterns in an experimental blunt chest trauma model in rats.MethodsExperimental blunt chest trauma was induced by a blast wave in rats, with subsequent analysis of its effects on the heart. The animals were subjected either to a sham or trauma procedure. Systemic markers for cardiac injury were determined after 24 h and 5 days. Postmortem analysis of heart tissue addressed structural injury and inflammation 24 h and 5 days after trauma.ResultsPlasma levels of extracellular histones were elevated 24 h and 5 days after blunt chest trauma compared to sham-treated animals. In the heart, up-regulation of interleukin-1β 24 h after trauma and increased myeloperoxidase activity 24 h and 5 days after trauma were accompanied by reduced complement C5a receptor-1 expression 24 h after trauma. Histological analysis revealed extravasation of erythrocytes and immunohistochemical analysis alteration of the pattern of the gap-junction protein connexin 43. Furthermore, a slight reduction of α-actinin and desmin expression in cardiac tissue was found after trauma together with a minor increase in sarcoplasmatic/endoplasmatic reticlulum calcium-ATPase (SERCA) expression.ConclusionsThe clinically highly relevant rat model of blast wave-induced blunt chest trauma is associated with cardiac inflammation and structural alterations in cardiac tissue.

Highlights

In the United States, approximately 30,000 patients with blunt cardiac trauma were recorded annually [1]
Up-regulation of interleukin-1β 24 h after trauma and increased myeloperoxidase activity 24 h and 5 days after trauma were accompanied by reduced complement complement component 5a (C5a) receptor-1 expression 24 h after trauma
The clinically highly relevant rat model of blast wave-induced blunt chest trauma is associated with cardiac inflammation and structural alterations in cardiac tissue

Summary

Introduction

In the United States, approximately 30,000 patients with blunt cardiac trauma were recorded annually [1]. Heart injury represents an independent predictor for a poor outcome [2], prolonged ventilation interval [3] and longer hospital stay [4], and is associated with dysrhythmias (including ventricular fibrillation) and sudden cardiac arrest [5, 6]. In the experimental setting of blast injury, bradycardia [8, 9] and decreased mean arterial pressure [10] [8, 11] have been reported. Some studies have postulated a reflexive nature of the blast wave-induced bradycardia, which could be prevented by vagotomy [11] or traumatic stimulation of arterial baroreceptors [12]. Effects of blunt cardiac injury appear to enhance the firmness of cardiac tissue, as demonstrated in a pig model of blunt chest trauma [13]

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