Objective:To investigate the expression of calcium sensing receptor（Ca SR）in vascular endothelial cells and the role of Ca SR expression in ischemia-reperfusion（I/R）injury model of rat axial flaps transplantation. Methods:I/R injury model was established on SD rats axial skin flaps based on superficial inferior epigastric vessels. After 3 h ischemia

all flaps were randomly divided into 3 groups（n=10 per group）:Ca Cl2

NPS2143+Ca Cl2 and normal saline（NS）. The necrosis ratios of skin flaps were evaluated;morphological changes were observed by HE staining;cell apoptosis was assessed by TUNEL staining. The expressions of Ca SR

Cleaved Casepase-3

Bax and Bcl-2 were detected by RT-PCR and immunohistochemistry

respectively

at 2 h and on 7 d after reperfusion.Results:Compared with the NS control group and NPS2143 +Ca Cl2 group

Ca Cl2 group acquired significantly more flap necrosis [（14.87±1.02）%

P=0.000]

TUNEL staining-positive cells（2 h :46. 960 ± 1. 965

7 d :48. 855 ± 3.550

P = 0. 000）

consistent with higher protein expression of Ca SR（2 h:0.157±0.011

7 d:0.129 ±0.015

PIHC=0.000;PPR-PCR=0.000）

Cleaved Casepase-3（2 h:0.101±0.020

7 d:0.098±0.011

PNS=0.046

PNPS2143 + Ca Cl2= 0. 000） and obvious brown staining of Bax

while almost no expression of Bcl-2. However compared with the NS control

NPS2143 + Ca Cl2 group manifested an anti-injury effect.Conclusion:The activation of Ca SR in the vascular endothelial cells may aggravate the I/R injury of of axial skin flaps while inhibition of Ca SR could deprive skin flaps of I/R injury.