Nitric Oxide Pathways and Evidence-Based Perturbations in Acute Pancreatitis

DiMagno, Matthew

doi:10.1159/000108956

Cited by 18 publications

(20 citation statements)

References 47 publications

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“…However, there is not agreement about its beneficial or detrimental role in this disease [57] ; moreover, an increase in NO has been suggested in SAP in humans [58] , but this issue is not yet clear [59] . We have demonstrated, by using an experimental model of necrotizing AP in rats, that NO and other va sodilators may exert a beneficial effect on SAP when they are administered before induction of pancreatitis [55] .…”

Section: From Local Pancreatic Damage To Systemic Effectsmentioning

confidence: 99%

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: 99%

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

García

Calvo²

2010

WJGPT

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“…Nitric oxide, a gaseous neurotransmitter, vasodilator and paracrine regulator is involved in the physiological functions of the pancreas including exocrine and endocrine secretion (insulin) as well as in regulating pancreatic microvascular blood flow [75]. It thus plays an important role in physiological and may possibly be involved in the development AP [76].…”

Section: Neurotransmitters and Oxidative Stress (Including Nitric Oximentioning

confidence: 99%

How does cigarette smoking cause acute pancreatitis?

Barreto

2016

Pancreatology

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“…It has been suggested that certain amount of NO production has beneficial effects in experimental edematous acute pancreatitis, but uncontrolled over-production of NO may be detrimental [176]. Endothelial NO synthase (eNOS) reduces the severity of the initial phase of experimental acute pancreatitis [177]. NO production and NOS expression seem to be differentially regulated temporally and in magnitude in the pancreas and lungs in response to caerulein hyperstimula- Fig.…”

Section: Nitrosative Stress In Acute Pancreatitismentioning

confidence: 99%

Cross-Talk between Oxidative Stress and Pro-Inflammatory Cytokines in Acute Pancreatitis: A Key Role for Protein Phosphatases

Escobar

Pereda²,

Arduini³

et al. 2009

CPD

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Acute pancreatitis is an acute inflammatory process localized in the pancreatic gland that frequently involves peripancreatic tissues. It is still under investigation why an episode of acute pancreatitis remains mild affecting only the pancreas or progresses to a severe form leading to multiple organ failure and death. Proinflammatory cytokines and oxidative stress play a pivotal role in the early pathophysiological events of the disease. Cytokines such as interleukin 1beta and tumor necrosis factor alpha initiate and propagate almost all consequences of the systemic inflammatory response syndrome. On the other hand, depletion of pancreatic glutathione is an early hallmark of acute pancreatitis and reactive oxygen species are also associated with the inflammatory process. Changes in thiol homestasis and redox signaling decisively contribute to amplification of the inflammatory cascade through mitogen activated protein kinase (MAP kinase) pathways. This review focuses on the relationship between oxidative stress, pro-inflammatory cytokines and MAP kinase/protein phosphatase pathways as major modulators of the inflammatory response in acute pancreatitis. Redox sensitive signal transduction mediated by inactivation of protein phosphatases, particularly protein tyrosin phosphatases, is highlighted.

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Nitric Oxide Pathways and Evidence-Based Perturbations in Acute Pancreatitis

Cited by 18 publications

References 47 publications

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

How does cigarette smoking cause acute pancreatitis?

Cross-Talk between Oxidative Stress and Pro-Inflammatory Cytokines in Acute Pancreatitis: A Key Role for Protein Phosphatases

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