Abstract

BackgroundPost-cardiac arrest syndrome, which has no specific curative treatment, contributes to the high mortality rate of victims who suffer traumatic cardiac arrest (TCA) and initially can be resuscitated. In the present study, we investigated the potential of ulinastatin to mitigate multiple organ injury after resuscitation in a swine TCA model.MethodsTwenty-one male pigs were subjected to hemodynamic shock (40% estimated blood loss in 20 min) followed by cardiac arrest (electrically induced ventricular fibrillation) and respiratory suspension for 5 min, and finally manual resuscitation. At 5 min after resuscitation, pigs were randomized to receive 80,000 U/kg ulinastatin (n = 7) or the same volume of saline (n = 9) in the TCA group. Pigs in the sham group (n = 5) were not exposed to bleeding or cardiac arrest. At baseline and at 1, 3, and 6 h after the return of spontaneous circulation, blood samples were collected and assayed for tumor necrosis factor-alpha, interleukin 6, and other indicators of organ injury. At 24 h after resuscitation, pigs were sacrificed and apoptosis levels were assessed in samples of heart, brain, kidney, and intestine.ResultsOne pig died in the ulinastatin group and one pig died in the TCA group; the remaining animals were included in the final analysis. TCA and resuscitation caused significant increases in multiple organ function biomarkers in serum, increases in tumor necrosis factor-alpha, and interleukin 6 in serum and increases in the extent of apoptosis in key organs. All these increases were lower in the ulinastatin group.ConclusionUlinastatin may attenuate multiple organ injury after TCA, which should be explored in clinical studies.

Highlights

  • Post-cardiac arrest syndrome, which has no specific curative treatment, contributes to the high mortality rate of victims who suffer traumatic cardiac arrest (TCA) and initially can be resuscitated

  • Baseline characteristics The three groups were similar at baseline in terms of body weight, Heart rate (HR), Mean aortic blood pressure (MAP), and, End-tidal carbon dioxide (ETCO2)

  • One pig died in the ulinastatin group and one

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Summary

Introduction

Post-cardiac arrest syndrome, which has no specific curative treatment, contributes to the high mortality rate of victims who suffer traumatic cardiac arrest (TCA) and initially can be resuscitated. Traumatic cardiac arrest (TCA) is associated with poor outcome; traditionally, only 0–3.7% of TCA patients could be resuscitated [1], though advances in damage control resuscitation and understanding of TCA pathophysiology have increased the success rate to 5.6% (0– 17%) [2], making it comparable to the rate with patients who suffer medical cardiac arrest [3]. A meta-analysis of randomized controlled trials concluded that ulinastatin can protect pulmonary tissue for patients undergoing cardiac surgery and reduce postoperative increases in the inflammatory agent’s tumor necrosis factor (TNF)-alpha, polymorphonuclear neutrophil elastase, and interleukin (IL)-6 and IL-8 [9]. Ulinastatin may be associated with a low incidence of acute kidney injury in patients undergoing robot-assisted laparoscopic partial nephrectomy or cardiac surgery [10, 11]

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