Inflammatory mediators in acute pancreatitis

Bhatia, Madhav; Brady, Mark; Shokuhi, Sheila; Christmas, Stephen E.; Neoptolemos, John P.; Slavin, John

doi:10.1002/(sici)1096-9896(200002)190:2<117::aid-path494>3.3.co;2-b

Cited by 147 publications

(225 citation statements)

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“…Although the mechanisms underlying hypotension associated with SAP are still not completely understood, a failure in the physi ological equilibrium between vasodilator and vasoconstric tor mediators has been proposed [54] . In two recent studies, we have analyzed whether an overwhelming production of vasodilators or a diminished response to vasoconstrictors occur in SAPassociated hypotension [55,56] and in the follow ing paragraphs we will summarize our main conclusions.…”

Section: From Local Pancreatic Damage To Systemic Effectsmentioning

confidence: 56%

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

García

Calvo²

2010

WJGPT

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Acute pancreatitis (AP) is a common and potentially lethal acute inflammatory process. Although the majority of patients have a mild episode of AP, 10%-20% develop a severe acute pancreatitis (SAP) and suffer systemic inflammatory response syndrome (SIRS) and/or pancreatic necrosis. The main aim of this article is to review the set of events, first localized in the pancreas, that lead to pancreatic inflammation and to the spread to other organs contributing to multiorganic shock. The early pathogenic mechanisms in SAP are not completely understood but both premature activation of enzymes inside the pancreas, related to an impaired cytosolic Ca 2+ homeostasis, as well as release of pancreatic enzymes into the bloodstream are considered important events in the onset of pancreatitis disease. Moreover, afferent fibers within the pancreas release neurotransmitters in response to tissue damage. The vasodilator effects of these neurotransmitters and the activation of pro-inflammatory substances play a crucial role in amplifying the inflammatory response, which leads to systemic manifestation of AP. Damage extension to other organs leads to SIRS, which is usually associated with cardiocirculatory physiology impairment and a hypotensive state. Hypotension is a risk factor for death and is associated with a significant hyporesponsiveness to vasoconstrictors. This indicates that stabilization of the patient, once this pathological situation has been established, would be a very difficult task. Therefore, it seems particularly necessary to understand the pathological mechanisms involved in the first phases of AP to avoid damage beyond the pancreas. Moreover, efforts must also be directed to identify those patients who are at risk of developing SAP.

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Section: From Local Pancreatic Damage To Systemic Effectsmentioning

confidence: 56%

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

García

Calvo²

2010

WJGPT

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“…Various medications directed at key stages of the pathophysiology are not clinically efficacious as indicated in the preceding experimental trials [23] . Therefore, therapies for preventing or reversing lung injury would be ideal for the treatment of AP [1,2,21,[24][25][26] .…”

Section: A B C Dmentioning

confidence: 99%

Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

Oge¹,

Tascilar²,

Güldeniz³

et al. 2007

WJG

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RESULTS:The mean pleural effusion volume, calculated LW/BW ratio, serum IL-6 and lung tissue MDA levels were significantly lower in EPO groups than in ANP groups. No statistically significant difference was observed in either serum or tissue values of IL-2 among the groups. The level of tumor necrosis factor-α (TNF-α) and IL-6 and accumulation of ox-LDL were evident in the lung tissues of ANP groups when compared to EPO groups, particularly at 72 h. Histopathological evaluation confirmed the improvement in lung injury parameters after exogenous EPO administration, particularly at 48 h and 72 h. C O N C L U S I O N : E P O a d m i n i s t r a t i o n l e a d s t o asignificant decrease in ALI parameters by inhibiting polymorphonuclear leukocyte (PMNL) accumulation, decreasing the levels of proinflammatory cytokines in circulation, preserving microvascular endothelial cell integrity and reducing oxidative stress-associated lipid peroxidation and therefore, can be regarded as a cytoprotective agent in ANP-induced ALI. INTRODUCTIONAcute pancreatitis (AP) is a life-threatening necroinflammatory disease with significant morbidity and mortality rates, especially when complicated by systemic inflammatory response syndrome (SIRS) and multiple organ failure (MODS) [1,2] . Death occurs in 60% of the patients within the first 6 d of disease onset and pulmonary complications including acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) Abstract AIM: To investigate the effect of exogenous erythropoietin (EPO) administration on acute lung injury (ALI) in an experimental model of sodium taurodeoxycholateinduced acute necrotizing pancreatitis (ANP). BASIC RESEARCH METHODS:Forty-seven male Wistar albino rats were randomly divided into 7 groups: sham group (n = 5), 3 ANP groups (n = 7 each) and 3 EPO groups (n = 7 each). ANP was induced by retrograde infusion of 5% sodium taurodeoxycholate into the common bile duct. Rats in EPO groups received 1000 U/kg intramuscular EPO immediately after induction of ANP. Rats in ANP groups were given 1 mL normal saline instead. All animals were sacrificed at postoperative 24 h, 48 h and 72 h. Serum amilase, IL-2, IL-6 and lung tissue malondialdehyde (MDA) were measured. Pleural effusion volume and lung/body weight (LW/BW) ratios were calculated. Tissue levels of TNF-α, IL-2 and IL-6 were screened immunohistochemically. Additionally, ox-LDL accumulation was assessed with immune-fluorescent staining. Histopathological alterations in the lungs were also scored.

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“…Recently PAF is deemed to be the key inflammatory mediator in SAP external secretion and local, systemic inflammatory reactions (Bhatia et al, 2000). Main actions of PAF (Kingsnorth, 1996;Wang et al, 1997;Roudebush et al, 2000;Reinhardt et al, 1999) include activation of platelet, promotion of platelet adhesion and aggregation, formation of thrombus; elevation of adhesion factor β 2 -integrin, change of endothelial cell skelemin, increase of capillary permeability, massive effusion of plasma, blood viscosity increase, slow down of blood flow, participation of ischemia-reperfusion injury; stimulation of vasoactive substances, generation of cytokine and inflammatory mediators, and so on.…”

Section: Platelet Activating Factor (Paf)mentioning

confidence: 99%

Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury

Zhang

Wang

Zhang

2007

J. Zhejiang Univ. - Sci. B

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Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis (SAP) in multiple organ injury is a hotspot in the surgical field. In clinical practice, the main complicated organ dysfunctions are shock, respiratory failure, renal failure, encephalopathy, with the rate of hepatic diseases being closely next to them. The hepatic injury caused by SAP cannot only aggravate the state of pancreatitis, but also develop into hepatic failure and cause patient death. Its complicated pathogenic mechanism is an obstacle in clinical treatment. Among many pathogenic factors, the changes of vasoactive substances, participation of inflammatory mediators as well as OFR (oxygen free radical), endotoxin, etc. may play important roles in its progression.

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Inflammatory mediators in acute pancreatitis

Cited by 147 publications

References 0 publications

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury

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