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

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.Electronic supplementary materialThe online version of this article (10.1186/s12871-018-0530-8) contains supplementary material, which is available to authorized users.

Assessment of Post-Resuscitation Intestinal Injury and Timing of Bacterial Translocation in Swine Anaesthetized With Propofol-Based Total Intravenous Anaesthesia

“…Although research has shown that the reperfused intestine is characterized by severe histological alterations, mucosal rupture, and increased permeability [23], we did not find significant differences in the intestinal mucosal injury score between the three groups. Our results are similar to those of Schroeder et al who reported a mild intestinal barrier damage and mild local intestinal inflammation within 24 h post-ROSC in a rat model of six-minute cardiac arrest [25]. The mild intestinal injury in the CA-CPR group may be also explained by the low dose of the administered adrenaline, which may have minimized the detrimental effect of the drug on mesenteric blood flow [26].…”

Fast Hypothermia Induced by Continuous Renal Replacement Therapy Alleviates Renal and Intestinal Injury after Cardiac Arrest in Swine

“…Evidence from pathologic processes, including decreasing the in ammation of tissues, suppressing oxidative stress and decreasing the level of apoptosis, was observed in tissues of kidney and intestine in the CRRT group. According to a growing body of literature, TNF-α and IL-6 are typical indexes to manifest the in ammatory response of the whole body or certain organs [36]. With a smaller elevation of TNF-α and IL-6, CRRT cooling might have a protective in uence by decreasing tissue in ammation in the kidney and small intestine.…”

Fast Hypothermia Induced by Continuous Renal Replacement Therapy Alleviates Renal and Intestinal Injury After Cardiac Arrest in Swine

“…Evidence from pathologic processes, including decreasing the in ammationof tissues, suppressing oxidative stress and decreasing the level of apoptosis,was observed in tissues of kidney and intestine in the CRRT group.According to a growing body of literature, TNF-α and IL-6 are typical indexes to manifest the in ammatory response of the whole body or certain organs [36]. With a smaller elevation of TNF-α and IL-6, CRRT cooling mighthave a protective in uence by decreasing tissue in ammation in the kidney and small intestine.…”