• Daniel C Schroeder, Alexandra C Maul, Esther Mahabir, Isabell Koxholt, Xiaowei Yan, Stephan A Padosch, Holger Herff, Insa Bultmann-Mellin, Anja Sterner-Kock, Thorsten Annecke, Tim Hucho, Bernd W Böttiger, and Maria Guschlbauer.
• Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Kerpener Str. 62, Cologne, Germany. Daniel.Schroeder@uk-koeln.de.
• BMC Anesthesiol. 2018 Jun 5; 18 (1): 6161.

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.

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