Diaphragmatic dysfunction in sepsis due to severe acute pancreatitis complicated by intra-abdominal hypertension

Liao, Weichao; Chen, Yanhong; Li, Hang-Yang; Wang, Tingting; Lan, Peng; Pan, Kong-Han; Ge, Huiqing; Xie, Qiang-min; Zhou, Jiancang

doi:10.1177/0300060517747163

Cited by 10 publications

(4 citation statements)

References 18 publications

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“…Sepsis declines the activity of oxygen-free radical scavengers in tissues, causing excessive oxygen-free radicals to be accumulated in tissues and can not be removed timely, and excessive oxygen-free radicals can induce lipid peroxidation, and then result in oxidative damage [ 28 ]. SOD and CAT, as antioxidant enzymes, are oxygen-free radical scavengers that present in the body [ 29 ]. MDA is the main product of lipid peroxidation [ 30 ], and a large number of oxygen free radicals in tissues can also activate apoptotic response and induce apoptosis [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats through the ERK/GSK-3β Signaling Axis

Zang

Song

Ying

2022

Evidence-Based Complementary and Alternative Medicine

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Objective. To explore the effect and possible mechanism of sufentanil on sepsis-induced myocardial injury and stress response in rats. Methods. The cecal ligation and puncture (CLP) method was utilized to establish the sepsis model of rats to explore the effect of sufentanil pretreatment with different concentrations on myocardial injury and oxidative stress in CLP rats. Echocardiogram was applied for detecting cardiac hemodynamic parameters in rats; hematoxylin and eosin (HE) staining as well as TUNEL staining was done for observing pathological changes of myocardial tissue and cardiomyocyte apoptosis in rats, respectively; biochemical testing and enzyme-linked immunosorbent assay (ELISA) were done for determining myocardial injury marker level in serum, oxidative stress substances in myocardial tissue, and neuroendocrine hormone level in serum of rats, respectively; finally, Western blot was performed for checking the expression level of ERK/GSK-3β signaling pathway-related proteins in myocardial tissue of rats. Results. A model of rat with sepsis-induced myocardial injury was constructed with the CLP method. Specifically, this rat model was characterized by obvious cardiac function and tissue damage, cardiomyocyte apoptosis, and oxidative stress response. Sufentanil pretreatment significantly improved cardiac function injury, alleviated pathological injury and oxidative stress response in myocardial tissue, and inhibited cardiomyocyte apoptosis. Specifically, after sufentanil pretreatment, left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) were downregulated, and left ventricular ejection fraction (LVEF) was upregulated; the level of B-type natriuretic peptide (BNP) of serum, creatine kinase isoenzyme (CK-MB), and troponin (cTnl) decreased; besides, malondialdehyde (MDA) level was declined, while activities of superoxide dismutase (SOD) and catalase (CAT) were increased. What is more, further mechanism exploration also revealed that sufentanil could reverse the activity of the sepsis-induced ERK/GSK-3β signaling pathway. Conclusion. Sufentanil has an obvious protective effect on myocardial injury and stress response in CLP rats, and this protective effect may be related to the activation of the ERK/GSK-3β signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats through the ERK/GSK-3β Signaling Axis

Zang

Song

Ying

2022

Evidence-Based Complementary and Alternative Medicine

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“…Severe acute pancreatitis complicated by IAH/ACS increases the risk for sepsis (Liao et al, 2018). The human intestine contains many microorganisms, and some of these Gram-negative bacteria can produce the toxin LPS.…”

Section: Discussionmentioning

confidence: 99%

Effect of Clostridium butyricum and Butyrate on Intestinal Barrier Functions: Study of a Rat Model of Severe Acute Pancreatitis With Intra-Abdominal Hypertension

et al. 2020

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Background/Aims: Severe acute pancreatitis (SAP) is associated with intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS), but treatment of these conditions is difficult. We studied a rat model of SAP + IAH to determine the effect of oral administration of Clostridium butyricum and butyrate (its major metabolite) on intestinal barrier functions.Methods: A total of 48 rats were assigned to four groups, with 12 rats per group: Sham, SAP+IAH, SAP+IAH+C. butyricum, and SAP + IAH + butyrate. SAP was induced by sodium taurocholate infusion into the biliopancreatic duct, intra-abdominal pressure (IAP), mortality was measured 24 h later, and then rats were euthanized. The plasma levels of several markers [amylase, diamine oxidase (DAO), fluorescein isothiocyanate (FITC)-dextran, tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-1β, IL-12, lipopolysaccharide (LPS)] and fecal butyric acid level were determined. The pancreas and intestine were examined using histology, and RT-PCR and Western blotting of intestinal tissues were used to measure the expression of six markers {tight junction proteins [zonula occludens protein-1 (ZO-1), claudin-1, claudin-2, occluding], matrix metalloproteinase 9 [MMP9], and TNF-α}. The gut flora of the rats was examined by 16S rRNA sequencing.Results: Induction of SAP + IAH altered several functions of the intestinal barrier, and enhanced intestinal permeability, decreased the levels of ZO-1, claudin-1, occludin, the richness and diversity of the microflora community, the relative abundance (RA) of Firmicutes, and the number of probiotic organisms. However, induction of SAP+IAH increased the expression of claudin-2, MMP9, and TNF-α, and the RA of Proteobacteria

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“…e antioxidants network consists of enzymes, such as catalase, glutathione peroxidase (GPx), thioredoxin reductases, superoxide dismutase (SOD), and soluble antioxidants such as glutathione and vitamin E [48]. It was found that GPx and SOD levels were significantly lower in the diaphragm of severe acute pancreatitis with intra-abdominal hypertension in a rat model [61]. Protein and mRNA expression levels of CuZnSOD, MnSOD, and GPx were found to be decreased or unaltered in the aged muscle even if its activity was increased [62].…”

Section: Mitochondrial Oxidative Stress In the Development Ofmentioning

confidence: 99%

Is Mitochondrial Oxidative Stress the Key Contributor to Diaphragm Atrophy and Dysfunction in Critically Ill Patients?

Duan

Bai

2020

Critical Care Research and Practice

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Diaphragm dysfunction is prevalent in the progress of respiratory dysfunction in various critical illnesses. Respiratory muscle weakness may result in insufficient ventilation, coughing reflection suppression, pulmonary infection, and difficulty in weaning off respirators. All of these further induce respiratory dysfunction and even threaten the patients’ survival. The potential mechanisms of diaphragm atrophy and dysfunction include impairment of myofiber protein anabolism, enhancement of myofiber protein degradation, release of inflammatory mediators, imbalance of metabolic hormones, myonuclear apoptosis, autophagy, and oxidative stress. Among these contributors, mitochondrial oxidative stress is strongly implicated to play a key role in the process as it modulates diaphragm protein synthesis and degradation, induces protein oxidation and functional alteration, enhances apoptosis and autophagy, reduces mitochondrial energy supply, and is regulated by inflammatory cytokines via related signaling molecules. This review aims to provide a concise overview of pathological mechanisms of diaphragmatic dysfunction in critically ill patients, with special emphasis on the role and modulating mechanisms of mitochondrial oxidative stress.

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Diaphragmatic dysfunction in sepsis due to severe acute pancreatitis complicated by intra-abdominal hypertension

Cited by 10 publications

References 18 publications

Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats through the ERK/GSK-3β Signaling Axis

Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats through the ERK/GSK-3β Signaling Axis

Effect of Clostridium butyricum and Butyrate on Intestinal Barrier Functions: Study of a Rat Model of Severe Acute Pancreatitis With Intra-Abdominal Hypertension

Is Mitochondrial Oxidative Stress the Key Contributor to Diaphragm Atrophy and Dysfunction in Critically Ill Patients?

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