Effect of Intraperitoneal Resuscitation With Different Concentrations of Sodium Pyruvate on Intestinal Ischemia Reperfusion Injury in Hemorrhagic Shock Rat

Jiang, Linlin; Zhang, Jingjing; Zhang, Zongze; He, Xiang-Hu; Dong-ling, Chen; Wang, Yanlin

doi:10.1097/shk.0000000000000515

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…12 Sodium pyruvate in different concentrations has different outcomes on intestinal ischemia reperfusion injury (IRI) in HS rats. 13 However, it remains unknown whether Pyr-PDS with different concentrations of pyruvate has different effects on acid–base disturbance and organ injury from HS.…”

Section: Introductionmentioning

confidence: 99%

Effect of peritoneal dialysis solution with different pyruvate concentrations on intestinal injury

Zhang

Shen

Deng

et al. 2020

Exp Biol Med (Maywood)

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To investigate the effects of direct peritoneal resuscitation with pyruvate-peritoneal dialysis solution (Pyr-PDS) of different concentrations combined with intravenous resuscitation on acid–base imbalance and intestinal ischemia reperfusion injury in rats with hemorrhagic shock. Sixty rats were randomly assigned to group SHAM, group intravenous resuscitation, and four direct peritoneal resuscitation groups combined with intravenous resuscitation: group NS, LA, PY1, and PY2, that is, normal saline, lactate-PDS (Lac-PDS), lower concentration Pyr-PDS (Pyr-PDS1), and higher concentration Pyr-PDS (Pyr-PDS2), respectively. Two hours after hemorrhagic shock and resuscitation, the pH, oxygen partial pressure, carbon dioxide partial pressure (PCO2), base excess, and bicarbonate ion concentration (HCO3−) of the arterial blood were measured. The intestinal mucosal damage index and intercellular adhesion molecule 1 (ICAM-1), tumor necrosis factor-α, interleukin-6, zonula occludens-1, claudin-1, and occludin levels in intestinal issues were detected. Two hours after resuscitation, group PY2 had higher mean arterial pressure, pH, oxygen partial pressure, and base excess and lower PCO2 of arterial blood than group PY1 ( P < 0.05). Tumor necrosis factor-α and interleukin-6 levels in group PY2 were significantly lower than those in group PY1 ( P < 0.05). Zonula occludens-1, claudin-1, and occludin expression levels were significantly higher in group PY2 than in group PY1 ( P < 0.05). Direct peritoneal resuscitation with Pyr-PDS2 combined with intravenous resuscitation enhanced the hemodynamics, improved the acid–base balance, and alleviated intestinal ischemia reperfusion injury from hemorrhagic shock and resuscitation in rats. The mechanisms might include correction of acidosis, inhibition of inflammatory response, enhancement of systemic immune status, regulation of intestinal epithelial permeability, and maintenance of intestinal mucosal barrier function. Impact statement Hemorrhagic shock is a life-threatening condition after trauma or during surgery. Acid–base imbalance and intestinal ischemia reperfusion injury are two significant causes in the pathogenetic process and multiple organ dysfunction. As a result, it is urgent and necessary to find an effective method of resuscitation in order to reverse the acid–base imbalance and protect organ function. This current study confirmed the protection against hypoxic acidosis and intestinal ischemia reperfusion injury by peritoneal resuscitation with pyruvate combined with intravenous resuscitation in rats with hemorrhagic shock. And the peritoneal dialysis solution with pyruvate of high concentration plays a crucial role in the process. It provided a new idea and possible direction of fluid resuscitation for alleviating organ injuries, protecting organ functions, and improving clinical prognosis after hemorrhagic shock and resuscitation.

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Section: Introductionmentioning

confidence: 99%

Effect of peritoneal dialysis solution with different pyruvate concentrations on intestinal injury

Zhang

Shen

Deng

et al. 2020

Exp Biol Med (Maywood)

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“…After CA, reestablishing the blood flow and oxygen supply are vital in heart and intestine. The reperfusion triggers a cascade of events that may inflict further injury and usually surpasses the initial ischemic damage (9,10). Intestinal I/R destroys the function of the mucosal barrier (11,12).…”

Section: Introductionmentioning

confidence: 99%

Maternally expressed 3 protects the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury via miR-34a-3p/sirtuin 1/nuclear factor kappa B signaling

Huang¹,

Pan²,

Du³

et al. 2021

Ann Transl Med

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Background: Cardiac arrest (CA), a common disease with a high mortality rate, is a leading cause of ischemia/reperfusion (I/R)-induced dysfunction of the intestinal barrier. Long non-coding RNAs (lncRNAs) play crucial roles in multiple pathological processes. However, the effect of the lncRNA maternally expressed 3 (MEG3) on intestinal I/R injury and the intestinal barrier has not been fully determined. Therefore, this study aimed to investigate the function of MEG3 in CA-induced intestinal barrier dysfunction. Methods:The oxygen and glucose deprivation (OGD) model in the human colorectal adenocarcinoma Caco-2 cells and in vivo cardiac arrest-induced intestinal barrier dysfunction model in Sprague-Dawley (SD) rats were established. The effect and underlying mechanism of MEG3 on the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury were analyzed by methyl thiazolyl tetrazolium (MTT) assays, Annexin V-FITC/PI apoptosis detection kit, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining, quantitative polymerase chain reaction (qPCR) assays, Western blot analysis, luciferase reporter gene assays, transepithelial electrical resistance (TEER) measurements, immunofluorescence analysis, and enzyme-linked immunosorbent assay (ELISA) assays.Results: Interestingly, we found that MEG3 could protect Caco-2 cells from oxygen-glucose deprivation (OGD)/reoxygenation-induced I/R injury by modulating cell proliferation and apoptosis. Moreover, MEG3 relieved OGD-induced intestinal barrier dysfunction in vitro, as demonstrated by its significant rescue effect on transepithelial electrical resistance and the expression of tight junction proteins such as occludin and claudin-1 (CLDN1), which were impaired in OGD-treated Caco-2 cells. Mechanistically, MEG3 inhibited the expression of inflammatory factors including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, interferon-gamma (IFN)-γ, inflammatory factors including interleukin (IL)-10, and transforming growth factor beta (TGFb)-1, as well as nuclear factor-kappa B (NF-κB) signaling. In response to OGD treatment in vitro, MEG3 also activated the expression of sirtuin 1 (SIRT1) by Caco-2 cells via sponging miR-34a-3p. Furthermore, MEG3 relieved CA-induced intestinal barrier dysfunction through NF-κB signaling in vivo.Conclusions: LncRNA MEG3 can protect the intestinal barrier from cardiac arrest-induced I/R injury via miR-34a-3p/SIRT1/NF-κB signaling. This finding provides new insight into the mechanism by which MEG3 restores intestinal barrier function following I/R injury, presenting it as a potential therapeutic candidate or strategy in intestinal injury.

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Perioperative Intestinal Injury: Etiology, Mechanism, and Prevention

Chen

Liu

2019

Severe Trauma and Sepsis

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Effect of Intraperitoneal Resuscitation With Different Concentrations of Sodium Pyruvate on Intestinal Ischemia Reperfusion Injury in Hemorrhagic Shock Rat

Cited by 4 publications

References 30 publications

Effect of peritoneal dialysis solution with different pyruvate concentrations on intestinal injury

Effect of peritoneal dialysis solution with different pyruvate concentrations on intestinal injury

Maternally expressed 3 protects the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury via miR-34a-3p/sirtuin 1/nuclear factor kappa B signaling

Perioperative Intestinal Injury: Etiology, Mechanism, and Prevention

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