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.