Evaluation of small intestinal damage in a rat model of 6\xa0Minutes cardiac arrest

Daniel C Schroeder,Stephan A Padosch,Esther Mahabir,Xiaowei Yan,Bernd W Böttiger,Holger Herff,Tim Hucho,Thorsten Annecke,Alexandra C Maul,Maria Guschlbauer,Anja Sterner-Kock,Insa Bultmann-Mellin,Isabell Koxholt

doi:10.1186/s12871-018-0530-8

Daniel C Schroeder, Stephan A Padosch + Show 11 more

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https://doi.org/10.1186/s12871-018-0530-8

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Abstract

BackgroundContribution of the small intestine to systemic inflammation after cardiac arrest (CA) is poorly understood. The objective was to evaluate whether an in vivo rat model of 6 min CA is suitable to initiate intestinal ischaemia-reperfusion-injury and to evaluate histomorphological changes and inflammatory processes in the small intestinal mucosa resp. in sera.MethodsAdult male Wistar rats were subjected to CA followed by cardio-pulmonary resuscitation. Proximal jejunum and serum was collected at 6 h, 24 h, 72 h and 7 d post return of spontaneous circulation (ROSC) and from a control group. The small intestine was evaluated histomorphologically. Cytokine concentrations were measured in jejunum lysates and sera.ResultsHistomorphological evaluation revealed a significant increase in mucosal damage in the jejunum at all timepoints compared to controls (p < 0.0001). In jejunal tissues, concentrations of IL-1α, IL-1β, IL-10, and TNF-α showed significant peaks at 24 h and were 1.5- to 5.7-fold higher than concentrations at 6 h and in the controls (p < 0.05). In serum, a significant higher amount of cytokine was detected only for IL-1β at 24 h post-ROSC compared to controls (15.78 vs. 9.76 pg/ml).ConclusionCA resulted in mild small intestinal tissue damage but not in systemic inflammation. A rat model of 6 min CA is not capable to comprehensively mimic a post cardiac arrest syndrome (PCAS). Whether there is a vital influence of the intestine on the PCAS still remains unclear.

Highlights

Contribution of the small intestine to systemic inflammation after cardiac arrest (CA) is poorly understood
TNF-α concentrations showed a significant time-dependent effect (p < 0.01) at 24 h post-return of spontaneous circulation (ROSC) compared to controls (1.5-fold increase, p < 0.01) and 6 h post-ROSC (1.4-fold increase, p < 0.05)
This study reveals three major findings: (i) mild intestinal barrier damage could be detected within 24 h in a rat model of 6 min CA. (ii) only mild local intestinal inflammation could be shown within 24 h after CA. (iii) a systemic inflammation and a potential contribution of the small intestine to systemic inflammation could not be simulated after 6 min of CA in rats

Summary

Introduction

Contribution of the small intestine to systemic inflammation after cardiac arrest (CA) is poorly understood. The objective was to evaluate whether an in vivo rat model of 6 min CA is suitable to initiate intestinal ischaemia-reperfusion-injury and to evaluate histomorphological changes and inflammatory processes in the small intestinal mucosa resp. Cardiac arrest (CA) results in transient systemic ischaemia followed by reperfusion as a consequence of successful resuscitation. Within hours to days, the characteristic systemic ischaemia-reperfusion-injury provokes a systemic inflammatory release known as sepsis-like- or post-cardiac arrest syndrome (PCAS) ending up in multiple organ failure [5, 6]. CA is a complex systemic ischaemia-reperfusion-injury with contribution of multiple independent tissue. Given that more than 30% of victims of CA show bacteremia upon presentation, the small intestine was discussed to be an immediate by-product of a systemic ischaemiareperfusion-injury [7, 8]

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