Published online Nov 1, 2004. doi: 10.3748/wjg.v10.i21.3185
Revised: March 29, 2004
Accepted: April 5, 2004
Published online: November 1, 2004
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.