Objectives to evaluate the effects of valsartan on myocardial no-reflow and its probable mechanism in signal transduction pathway.
Methods Fifty-six male SD rats were randomly assigned to four groups: shame group, ischaemia and reperfusion group, valsartan group (valsartan 10mg/kg) and valsartan + LY294002 group (valsartan 10mg/kg, LY294002 0.3mg/kg). All rats, except for those in shame group, received occlusion of left anterior descending artery (LAD) for 60 minutes followed by 120 minutes of reperfusion. Valsartan (15 mg/kg) intravenous administration 15 minutes before reperfusion, and LY294002 (0.3 mg/kg ) intravenous administration 5 minutes before reperfusion. Different myocardium regions of ischaemia, no- reflow and infarction were recognised and assessed according to Evans blue dye, thioflavin S fluorescent dye and triphenyltetrazolium chloride (TTC) staining techniques, respectively. Serum CK- MB were detected after experiment. The expression of p-akt, akt, p-eNOS and eNOS was determined by western blotting.
Results Valsartan significantly elevated the expression of p-akt and p-eNOS, reduced CK-MB activity, and reduced the no-reflow (31.26 ± 2.83 vs 21.60 ± 3.29, P<0.01) and necrosis areas (40.16 ± 4.19% vs 27.93 ± 4.57%, P<0.01). However, these effects were reversed by LY294002.
Conclusions Valsartan can reduce the area of myocardial no-reflow after ischaemia-reperfusion. This beneficial effect is dependant on PI3K-akt-eNOS signal transduction pathway.