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AIM: To investigate the fluid shear stress induced changes of [Ca2+]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 [Ca2+]i showed biphasic changes. The shear rate changed from low to high,[Ca2+]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 [Ca2+]i level and the alteration of fluid shear stress in regional microcirculation of AP.CONCLUSION: The increase of [Ca2+]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 [Ca2+]i may play a crucial role in pancreatic microcirculatory failure of AP.