| Acute necrotjzing pancreatitis is a common disease characterized as an inflammatory response. Once it occurred it would cause the local and systemic response and involving other organs, particularly the lungs, kidneys, and liver. Clinically detectable signs of lung injury are seen in up to 70% of patients with acute necrotizing pancreatitis, which is the most common complication, many of them developed into adult respiratory distress syndrome (ARDS). It is the main cause of death at an early stage of acute necrotizing pancreatitis.It is still unknown that how the inflammation disseminated from the local pancreas into the systematic and caused the systemic inflammatory response syndrome (SIRS) when the acute necrotizing pancreatitis occurred. Cytokines seem to play the key role in it. The activation of leukocyte mediated by the cytokines is the direct result of SIRS.The mechanism of lung injury associated with acute necrotizing pancreatitis remains unclear. It would be sure from the present study that the aggregation of neutrophils into the lungs seems to be the final common pathway that leads to lung damage.The recent years study showed that activation of alveolar macrophages is the important way of lung injury of acute necrotizing pancreatitis. The macrophages released many proinflammatory mediators such as cytokines, nitric oxide ( NO ) and arachidonic acid metabolities after their activation in the course of acute necrotizing pancreatitis, which would cause'the aggregation of neutrophils into the lungs and induced the lung injury.ARDS is an acute disseminated injury of pulmonary vessel endothelium and alveolar endothelium and will cause the respiratory failure finally. Now it is generally thought that the substance of acute lung injury (ALI) and ARDS is pulmonary capillary damage caused by pulmonary local inflammation response involved by many cytokines and out of control of the inflammation response. One distinctive pathological feature of ALI is the aggregation of large amounts of leukocyte, which is mainly polymorphonuclear neutrophils and macrophages. The emigration from the vessel and activation of leukocyte is a multiple procedure continuous process. This series complicated progress depends on three basic conditions; the role of cytokines, activation of leukocyte and vascular endothelium and the expression of adhesive molecule.The present study showed that the excessive production of inflammatory cytokines had relation to the lung injury associated with acute necrotizing pancreatitis and tumor necrosis factor alpha (TNFa) had direct relation to the occurrence of ARDS. But it remains unclear that how TNFa worked.NO participated in the pathophysiology of infection, immune, the brain vessel disease and liver cirrhosis as a new intracellular messenger molecule and plays an important role in regulation of physiology and pathology of body. The civil and foreign investigators have paid attention to its role in acute pancreatitis. However, its role in lung injury is still unknown. The conclusions of some experiments are paradoxical. 0'Donovan et al suggested that in vivo, nitric oxide inhibited pancreatitis - induced lung injury and application of inducible nitric oxide synthase (iNOS) inhibitor would aggravate lung injury, possibly in part by inhibiting pulmonary neutrophil influx. Closa D et al demonstrated that alveolar macrophages could be activated in acute pancreatitis and produced NO. NO can promote the aggregation of neutrophils in alveolar cavity, increase the permeability of pulmonary capilla'ry and lead to pulmonary edema as a proinflammatory mediator. So it led to lung injury. Tsukahara Y et al suggested that alveolar macrophage - derived NO contributed to lung injury during early phase of acute pancreatitis. Administration of NOS inhibitor prevented lung injury. In light of these, it should be deeply discussed for the role of NO in lung injury associatedwith acute pancreatitis.Gadolinium, a rare earth element, can inactivate macrophages and suppress macrophage media...
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