Abstract: Objective  To investigate the expressions and mechanisms of  zinc and zinc transporter (Zip13) in the myocardium of rats with hypersaltinduced left ventricular diastolic dysfunction（LVDD）.  Methods   A total of 36 Dahl saltsensitive (DSS) rats were randomly divided into model group  (a highsalt diet containing 8% NaCl,  n=22) and  control group (a highsalt diet containing 0.3% NaCl,  n=14）.  The Vevo 2100 ultrasound equipment for small animals was used to evaluate the cardiac function of rats in each group.  The concentrations of zinc ions in serum and myocardial tissues were determined by inductively coupled plasma optical emission spectroscopy(ICPDES).  The protein and mRNA expressions of Zip13 in the myocardium were detected by Western blot and RT qPCR methods. Results  Compared with the control group,  the model group showed significant increase in left ventricular posterior wall at enddiastole (LVPWd),  left ventricular enddiastolic dimension (LVDd),  left ventricular end systolic dimension (LVSd),  left ventricular posterior wall at endsystole (LVPWs),   left ventricular mass (LVM) and  ratio of LVM to weight (LVM/weight)(P<0.05).  The concentration of zinc ions in myocardial tissues significantly increased,  while that in serum decreased obviously(P<0.05).  The expressions of Zip13 protein and mRNA in myocardial tissues of the model group significantly increased (P<0.05).Conclusion  LVDD rats had a zinc homeostasis with elevated myocardial zinc ion concentration.  And the expressions of Zip13 protein and mRNA were upregulated,  which indicated that Zip 13 may help  regulate and correct the zinc homeostasis and inhibited myocardial remodeling of LVDD.  The specific mechanism needs to be further studied.

Key words: heart failure, , diastolic, zinc transporter; , zinc homeostasis; , myocardial remodeling