OBJECTIVE: To probe into the effect of dexmedetomidine on myocardial autophagy in rats with myocardial reperfusion by regulating PI3 K/AKT pathway. METHODS: 48 model rats with myocardial reperfusion were prepared and divided into model group

dexmedetomidine

LY294002（ P13 K inhibitor） group and dexmedetomidine+LY294002 group via random number table

with 12 rats in each group

and another 12 rats were set as sham-operation group. After grouping

2

3

5-Tri Phenyte-trazoliumchloride（ TTC） staining was adopted to detect myocardial infarction in each group

TUNEL staining was adopted to detect myocardial apoptosis in each group; enzyme linked immunosorbent assay was used to detect the contents of creatine kinase isoenzyme（ CK-MB） and troponin I（ c TnⅠ） in rats

Western blotting was used to detect the expression of autophagy-related protein（ Beclin-1

LC3-Ⅰ

LC3-Ⅱ and P62） and PI3 K/Akt pathway protein（ P-PI3 K/PI3 K and P-Akt/Akt） in myocardial tissue. RESULTS: Compared with sham-operation group

the area of myocardial infarction

contents of CK-MB and c TnⅠ

expression of Beclin-1

LC3-Ⅱ and P62 protein of model group were significantly higher

while the P-PI3 K/PI3 K and P-Akt/Akt were significantly lower

with statistically significantly differences（ P < 0. 05）. Compared with model group

the area of myocardial infarction

contents of CK-MB and c Tn Ⅰ

expression of Beclin-1

LC3-Ⅱ and P62 protein of dexmedetomidine group were significantly lower

while the P-PI3 K/PI3 K and P-Akt/Akt were significantly higher

with statistically significantly differences（ P<0. 05）; the area of myocardial infarction

contents of CK-MB and c TnⅠ

expression of Beclin-1

LC3-Ⅱ and P62 protein of LY294002 group were significantly higher

while the P-PI3 K/PI3 K and P-Akt/Akt were significantly lower

with statistically significantly differences（ P < 0. 05）. Compared with dexmedetomidine group

the area of myocardial infarction

contents of CK-MB and c Tn Ⅰ

expression of Beclin-1

LC3-Ⅱ and P62 protein of dexmedetomidine+LY294002 group were significantly higher

while the P-PI3 K/PI3 K and P-Akt/Akt were significantly lower

with statistically significantly differences（ P < 0. 05）. Compared with LY294002 group

the area of myocardial infarction

contents of CK-MB and c Tn Ⅰ

expression of Beclin-1

LC3-Ⅱ and P62 protein of dexmedetomidine+LY294002 group were significantly lower

while the P-PI3 K/PI3 K and P-Akt/Akt were significantly higher

with statistically significantly differences（ P < 0. 05）. There was no statistical significance in differences in expression levels of LC3-Ⅰ protein in myocardial tissue among various groups（ P > 0. 05）.CONCLUSIONS: Dexmedetomidine can weaken myocardial autophagy in rats with myocardial ischemia reperfusion by activating PI3 K/Akt pathway

so as to protect myocardial tissue from damage.