EFFECT OF THE BOVINE HEMOGLOBIN SOLUTION (HBOC-301) WITH AND WITHOUT ISOVOLEMIC HEMODILUTION ON PANCREATIC TISSUE OXYGENATION, PANCREATIC MICROCIRCULATION AND SURVIVAL IN PIGS WITH SEVERE ACUTE PANCREATITIS

Pancreas ◽  
2005 ◽  
Vol 31 (4) ◽  
pp. 449-450
Author(s):  
H Kleinhans ◽  
O Mann ◽  
M Freitag ◽  
C Schneider ◽  
S Petri ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Tissue Oxygenation ◽  
Pancreatic Tissue ◽  
Bovine Hemoglobin ◽  
Hemoglobin Solution ◽  
Isovolemic Hemodilution

Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells (huMSCs) Carrying MicroRNA-342 Relieve Protect Severe Acute Pancreatitis Injury (SAP)

2021 ◽  
Vol 11 (9) ◽  
pp. 1838-1843
Author(s):  
Xiaohong Zhou ◽  
Xuzhong Hao ◽  
Feifei He
Keyword(s):  
Stem Cells ◽  
Acute Pancreatitis ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Severe Acute Pancreatitis ◽  
Pancreatic Tissue ◽  
Inflammatory Factors ◽  
Control Group ◽  
Human Umbilical Cord Blood ◽  
Human Umbilical Cord

To investigate whether exosomes (exo) derived from human umbilical cord mesenchymal stem cells (huMSCs) and microRNA (miRNA)-342 have a protective effect on severe acute pancreatitis (SAP). Human umbilical cord blood was collected to extract huMSC-exo. With sham-operated mice as control group (n = 10), the other mice were induced to SAP model (n = 20), while 10 of the SAP mice received treatment with huMSC-exo. ELISA was performed to determine amylase and TAP level as well as inflammatory factors and HE staining to evaluate pathological changes of pancreatic tissue. The expression of miR-342 and Shh, Ptchl, and Smo in the Hh signal pathway was detected using RT-qPCR. The expression of miR-342 and the mRNA expression of Shh, Ptchl, and Smo was higher than that in model group (p < 0.05). The level of serum amylase, trypsinogen, and IFN-γ,Fasl, and IL-6 was upregulated in pancreas tissues of SAP mice relative to healthy mice, but their levels were decreased upon treatment with huMSC-exo and slightly higher than those of the control group, just not significantly. Collectively, the huMSC-exo may activate the Hh signaling pathway by regulating the expression of miR-342 increasing the expression of Shh, Ptchl, and Smo, and thereby healing of damaged pancreatic tissues in SAP.

scholarly journals CT Image Changes of Severe Acute Pancreatitis Based on Smart Electronic Medical Augmented Reality in Nursing Practice

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Defen Zhang ◽  
Shifang Mao ◽  
Siyou Lan ◽  
Chengli Zhou ◽  
Xiaoyan Liu
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Pancreatic Juice ◽  
Nursing Practice ◽  
Imaging System ◽  
Pancreatic Tissue ◽  
Ct Imaging ◽  
Pancreatic Ducts ◽  
Ct Image ◽  
Internal Drainage

Severe acute pancreatitis (SAP) is traditionally treated with chemical analysis. Faced with the increasing maturity of CT imaging technology, it is necessary to use more advantageous CT imaging to treat SAP. In this article, 72 SAP patients admitted to the Affiliated Hospital of Southwest Medical University were selected for study, of which 62 were severely ill, 8 were exacerbated, and 2 changed from severe to mild. This article combines the patient’s case records and related CT images during treatment from the perspective of nursing and conducts nursing research on the application of CT image changes in severe acute pancreatitis in nursing practice. CT image processing uses CT imaging system workstation (DICOM). The results of the study showed that, in the care of patients, 21 cases had recurrence after internal drainage, and the cure rate was 91.1%. Internal drainage is an effective way to treat SAP. The higher the incidence of pancreatitis, the more likely it is to relapse after SAP internal drainage, which may be related to repeated episodes of pancreatitis and repeated inflammation of the pancreas and pancreatic duct damage. 4 of the relapsed cases in this article are postchronic pancreatitis SAP, and the relapsed cases account for 50% of the chronic pancreatic cases. This may be due to chronic fibrosis of the branched and main pancreatic ducts, continuous abnormal pancreatic juice drainage. Therefore, it is necessary to further explore the prognosis of different causes of SAP. In terms of complication care, the overall complication rate was 16.6%. One patient died of postoperative hemorrhage. Analysis of the causes of cyst recurrence and complications may be closely related to the mechanism of the occurrence and development of SAP. The initiating factor of SAP is that the pancreatic tissue is damaged due to inflammation, trauma, or microcirculation disorder, and then the pancreatic juice leaks out of the pancreas, wrapping the pancreatic juice; it takes a certain time for the capsule of fibrous knot tissue to form and strengthen.

scholarly journals Parenteral nutrition versus enteral nutrition in severe acute pancreatitis

2010 ◽  
Vol 25 (5) ◽  
pp. 449-454 ◽  
Author(s):  
Josiel Paiva Vieira ◽  
Gutemberg Fernandes de Araújo ◽  
José Raimundo Araújo de Azevedo ◽  
Alberto Goldenberg ◽  
Marcelo Moura Linhares
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Nutritional Support ◽  
Average Length ◽  
Infectious Complications ◽  
Pancreatic Tissue ◽  
Septic Complications ◽  
Disease Etiology ◽  
The Difference ◽  
Length Of Hospitalization

PURPOSE: To compare the effect of parenteral versus enteral nutritional support in severe acute pancreatitis, with respect to efficacy, safety, morbidity, mortality and length of hospitalization. METHODS: The study was comprised of 31 patients, divided into a parenteral group (n=16) and an enteral group (n=15), who met severity criteria for abdominal tomography (Balthazar classes C, D, and E). The patients were compared by demographics, disease etiology, antibiotic prophylaxis, use or not of somatostatin, nutritional support, complications and disease progression. RESULTS: There was no statistical difference in the average duration of nutritional support, somatostatin, or antibiotics in the two groups. Imipenem was the drug of choice for prophylaxis of pancreatic infections in both groups. More complications occurred in the parenteral group, although the difference was not statistically significant (p=0.10). Infectious complications, such as catheter sepsis and infections of the pancreatic tissue, were significantly more frequent in the parenteral group (p=0.006). There was no difference in average length of hospitalization in the two groups. There were three deaths in the parenteral group and none in the enteral group. CONCLUSION: Enteral nutritional support is associated with fewer septic complications compared to parenteral nutritional support.

scholarly journals Aspirin Protects against Acinar Cells Necrosis in Severe Acute Pancreatitis in Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Guotao Lu ◽  
Zhihui Tong ◽  
Yanbing Ding ◽  
Jinjiao Liu ◽  
Yiyuan Pan ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Acinar Cell ◽  
Acinar Cells ◽  
Pancreatic Tissue ◽  
Pancreatic Acinar Cell ◽  
Cell Nuclei ◽  
Associated Proteins ◽  
Anti Inflammatory

Aspirin has a clear anti-inflammatory effect and is used as an anti-inflammatory agent for both acute and long-term inflammation. Previous study has indicated that aspirin alleviated acute pancreatitis induced by caerulein in rat. However, the role of aspirin on severe acute pancreatitis (SAP) and the necrosis of pancreatic acinar cell are not yet clear. The aim of this study was to determine the effects of aspirin treatment on a SAP model induced by caerulein combined with Lipopolysaccharide. We found that aspirin reduced serum amylase and lipase levels, decreased the MPO activity, and alleviated the histopathological manifestations of pancreas and pancreatitis-associated lung injury. Proinflammatory cytokines were decreased and the expression of NF-κB p65 in acinar cell nuclei was suppressed after aspirin treatment. Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased. Intriguingly, the downregulation of critical necrosis associated proteins RIP1, RIP3, and p-MLKL was observed; what is more, we additionally found that aspirin reduced the COX level of pancreatic tissue. In conclusion, our data showed that aspirin could protect pancreatic acinar cell against necrosis and reduce the severity of SAP. Clinically, aspirin may potentially be a therapeutic intervention for SAP.

scholarly journals HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Runkuan Yang ◽  
Jyrki Tenhunen ◽  
Tor Inge Tonnessen
Keyword(s):  
Acute Pancreatitis ◽  
Inflammatory Cytokines ◽  
Severe Acute Pancreatitis ◽  
Systemic Inflammation ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Mucosal Injury ◽  
Pancreatic Tissue ◽  
Multiple Organ ◽  
Hmgb1 Level

Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extrapancreatic organs dysfunction; however, the underlying mechanisms are still not clear. Ischemia-reperfusion, circulating inflammatory cytokines, and possible bile cytokines significantly contribute to gut mucosal injury and intestinal bacterial translocation (BT) during SAP. Circulating HMGB1 level is significantly increased in SAP patients and HMGB1 is an important factor that mediates (at least partly) gut BT during SAP. Gut BT plays a critical role in triggering/inducing systemic inflammation/sepsis in critical illness, and profound systemic inflammatory response syndrome (SIRS) can lead to multiple organ dysfunction syndrome (MODS) during SAP, and systemic inflammation with multiorgan dysfunction is the cause of death in experimental SAP. Therefore, HMGB1 is an important factor that links gut BT and systemic inflammation. Furthermore, HMGB1 significantly contributes to multiple organ injuries. The SAP patients also have significantly increased circulating histones and cell-free DNAs levels, which can reflect the disease severity and contribute to multiple organ injuries in SAP. Hepatic Kupffer cells (KCs) are the predominant source of circulating inflammatory cytokines in SAP, and new evidence indicates that hepatocyte is another important source of circulating HMGB1 in SAP; therefore, treating the liver injury is important in SAP.

scholarly journals Qingyi decoction attenuates severe acute pancreatitis in rats via inhibition of inflammation and protection of the intestinal barrier

2019 ◽  
Vol 47 (5) ◽  
pp. 2215-2227 ◽  
Author(s):  
Song Su ◽  
Tiancheng Liang ◽  
Xiang Zhou ◽  
Kai He ◽  
Bo Li ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Sodium Taurocholate ◽  
Intestinal Barrier ◽  
Pancreatic Tissue ◽  
Small Intestinal Mucosa ◽  
Barrier Dysfunction ◽  
Ileal Mucosa ◽  
Inflammatory Infiltration ◽  
Tnf Α

Objective Qingyi decoction (QYD) has beneficial effects in severe acute pancreatitis (SAP). We assessed the therapeutic effect and mechanisms of QYD in SAP. Methods A rat model of SAP was induced by pancreatic ductal injection of sodium taurocholate. QYD was administered intragastrically immediately postoperatively and once every 12 hours. Serum amylase, endotoxin, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and D-lactate levels were measured at 12, 24, and 48 hours. Histological changes in the pancreas and ileum were analyzed. Expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-κB p65), Toll-like receptor 4 (TLR4), and zonula occludens-1 (ZO-1) in the small intestinal mucosa was also assessed. Results Pancreatic tissue showed extracellular space expansion, inflammatory infiltration, vessels with necrotic walls, and hemorrhage. Ileal tissue showed hemorrhage, inflammatory infiltration, and ileal mucosa destruction. These histological features were dramatically improved by QYD. Increased serum levels of amylase, endotoxin, TNF-α, IL-6, and D-lactic acid were significantly decreased by QYD administration. Increased expression of NF-κB p65 and TLR4 and decreased expression of ZO-1 in the ileal mucosa were also restored to normal levels by QYD treatment. Conclusion QYD alleviates SAP by reducing intestinal barrier dysfunction, inhibiting intestinal bacteria and endotoxin translocation, and preventing NF-κB activation.

Mesenchymal Stem Cells Inhibits the Shh/GLi (Sonic Hedgehog/GLi) Axis and Promotes Repair of Tissue Injury in Severe Acute Pancreatitis

2022 ◽  
Vol 12 (2) ◽  
pp. 386-392
Author(s):  
Bo Qian ◽  
Hongmei Zhang ◽  
Jijun Zhang ◽  
Chao Bai ◽  
Wencai Sun
Keyword(s):  
Stem Cells ◽  
Acute Pancreatitis ◽  
Mesenchymal Stem Cells ◽  
Severe Acute Pancreatitis ◽  
Sonic Hedgehog ◽  
Tissue Injury ◽  
Pancreatic Tissue ◽  
Control Group ◽  
Tissue Necrosis ◽  
Regulated Expression

Mesenchymal stem cells (MSCs) are indicated to severe pancreatitis (SAP), whilst level of Shh/GLi axis varies in severe acute pancreatitis (SAP). However, little is known the interaction between MSCs and Shh in SAP. In this study, we established animal model of SAP in 10 rats and transplanted MSCs into 10 rats, with another 10 sham-operated rats as control group. The pathological changes of rat pancreatic tissue were observed. ELISA was conducted to determine the MPO level of pancreatic inflammation, and Western blot to detect the expression level of Shh, Gli1 and Gli2 in tissues. Administration of MSCs remarkably alleviated the pancreatic tissue necrosis and inflammation and decreased blood loss in SAP rats. Up-regulated expression of Shh, Gli1 and Gli2 was observed in SAP tissues when compared to tissues in control group, but their expressions declined in the presence of MSCs, and 24 hour later returned to normal levels. Collectively, MSCs regulates the balance of Shh/GLi axis by decreasing Shh and Gli1, thereby attenuating progression and symptoms of SAP.

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