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Changes of cytosolic [Ca^(2+)]i in neutrophils in pancreatic microcirculation of rats with caerulein-induced acute pancreatitis under fluid shear stress 被引量:5

Changes of cytosolic [Ca^(2+)]i in neutrophils in pancreatic microcirculation of rats with caerulein-induced acute pancreatitis under fluid shear stress
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摘要 AIM: To investigate the fluid shear stress induced changes of [Ca^2+]i in neutrophils in pancreatic microcirculation of experimental acute pancreatitis (AP).METHODS: Wistar rats (n = 36) were randomized into three groups. A model of AP was established by subcutaneous injection of caerulein. Low-shear 30 viscometer was used to provide steady fluid shear stress on separated neutrophils. The mean fluorescent intensity tested by flow cytometry was used as the indication of [Ca2+]i quantity.RESULTS: Under steady shear, cytosolic [Ca^2+]i showed biphasic changes. The shear rate changed from low to high, [Ca^2+]i in different groups decreased slightly and then increased gradually to a high level (P<0.05). A close correlation was observed between the cytosolic [Ca^2+]i level and the alteration of fluid shear stress in regional microcirculation of AP. CONCLUSION: The increase of [Ca^2+]i is highly related to the activation of neutrophils, which contributes to neutrophil adhesion to endothelium in the early phase of AP. The effect of fluid shear stress on [Ca^2+]i may play a crucial role in pancreatic microcirculatory failure of AP. AIM:To investigate the fluid shear stress induced changes of[Ca^(2+)]i in neutrophils in pancreatic microcirculation of experimental acute pancreatitis(AP). METHODS:Wistar rats(n=36)were randomized into three groups.A model of AP was established by subcutaneous injection of caerulein.Low-shear 30 viscometer was used to provide steady fluid shear stress on separated neutrophils. The mean fluorescent intensity tested by flow cytometry was used as the indication of[Ca^(2+)]i quantity. RESULTS:Under steady shear,cytosolic[Ca^(2+)]i showed biphasic changes.The shear rate changed from low to high, [Ca^(2+)]i in different groups decreased slightly and then increased gradually to a high level(P<0.05).A close correlation was observed between the cytosolic[Ca^(2+)]i level and the alteration of fluid shear stress in regional microcirculation of AP. CONCLUSION:The increase of[Ca^(2+)]i is highly related to the activation of neutrophils,which contributes to neutrophil adhesion to endothelium in the early phase of AP.The effect of fluid shear stress on[Ca^(2+)]i may play a crucial role in pancreatic microcirculatory failure of AP.
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2004年第21期3185-3187,共3页 世界胃肠病学杂志(英文版)
基金 Supported by the National Natural Science Foundation of China,No.39770722 and the Key Project of National Outstanding Youth Foundation of China,No.39925032
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  • 1Vollmar B, Menger MD. Microcirculatory dysfunction in acute pancreatitis. A new concept of pathogenesis involving vasomotion-associated arteriolar constriction and dilation.Pancreatology 2003; 3:181-190.
  • 2Chen HM, Sunamura M, Shibuya K, Yamauchi JI, Sakai Y,Fukuyama S, Mikami Y, Takeda K, Matsuno S. Early microcirculatory derangement in mild and severe pancreatitis models in mice. Surg Today 2001; 31:634-642.
  • 3Menger MD, Plusczyk T, Vollmar B. Microcirculatory derangements in acute pancreatitis. J Hepatobiliary Pancreat Surg 2001;8:187-194.
  • 4Gomez-Cambronero LG, Sabater L, Pereda J, Cassinello N,Camps B, Vina J, Sastre J. Role of cytokines and oxidative stress in the pathophysiology of acute pancreatitis: therapeutical implications. Curr Drug Targets Inflamm Allergy 2002; 1:393-403.
  • 5Frossard JL. Pathophysiology of acute pancreatitis: a multistep disease. Acta Gastroenterol Belg 2003; 66:166-173.
  • 6Makhija R, Kingsnorth AN. Cytokine storm in acute pancreatitis.J Hepatobiliary Pancreat Surg 2002; 9:401-410.
  • 7Weber CK, Adler G. From acinar cell damage to systemic inflammatory response: current concepts in pancreatitis.Pancreatology 2001; 1:356-362.
  • 8Sutton R, Criddle D, Raraty MG, Tepikin A, Neoptolemos JP, Petersen OH. Signal transduction, calcium and acute pancreatitis. Pancreatology 2003; 3:497-505.
  • 9Parekh AB. Calcium signaling and acute pancreatitis: specific response to a promiscuous messenger. Proc Natl Acad Sci U S A 2000; 97:12933~12934.
  • 10Raraty MG, Petersen OH, Sutton R, Neoptolemos JP. Intracellular free ionized calcium in the pathogenesis of acute pancreatitis. Baillieres Best Pract Res Clin Gastroenterol 1999; 13:241-251.

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