Effect of vanillic acid on ischemia-reperfusion of isolated rat heart: Hemodynamic parameters and infarct size assays.

Vanillic acid is an oxidized form of vanillin produced during the conversion of vanillin to ferulic acid and has free radical scavenging, antioxidant and anti-inflammatory properties. In this study, we investigated the effects of vanillic acid on hemodynamic parameters and infarct size in ischemia-reperfusion of isolated rat heart. Adult male Sprague Dawley rats were randomly divided into control and treatment groups (n = 10). The treatment groups were administered vanillic acid 5, 10 and 20 mg/kg orally for 10 days, then the hearts isolated and were exposed to 30 min ischemia and 1 h reperfusion, using langendorff apparatus. The effects of vanillic acid, on left ventricular developed pressure (LVDP), LV end diastolic pressure (LVEDP), LV pressure (LVP), peak rate of rise and fall of LVP (±dp/dt), coronary flow (CF), rate pressure product (RPP) and infarct size were examined. Rats administered with vanillic acid (10 and 20 mg/kg), displayed significantly improved recovery of LVEDP, RPP, LVDP, LVP and ± dp/dt as compared to control group. There was also significant beneficial effect of these two doses to reduce infarct size. Our results suggest that vanillic acid can effectively improve ventricular function and reduce infarct size in ischemia-reperfusion of isolated rat heart.

Effects of losartan and vanillic Acid co-administration on ischemia-reperfusion-induced oxidative stress in isolated rat heart.

BACKGROUND: Experimental studies have demonstrated that angiotensin II (ANG-II)-induced oxidative stress contributes to the pathogenesis of I/R injury. OBJECTIVES: This study was aimed to investigate the protective effects of co-administration of losartan, as a selective ANG-II type 1 receptor (AT1R) blocker, and vanillic acid (VA), as an antioxidant, in I/R-induced oxidative stress in isolated rat heart. MATERIALS AND METHODS: Adult male Wistar rats were randomly divided to sham, control, and five treatment groups (n = 10). Two doses of VA (5 and 10 mg/kg), one dose of losartan (20 mg/kg) alone, and one dose of losartan in combination with either doses of VA were administered orally for 10 days. The hearts were isolated and exposed to 30 minutes ischemia and 60 minutes reperfusion, using Langendorff apparatus. I/R-induced myocardial injury was assessed by estimating the release of lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and myocardial creatine kinase (CK-MB) in coronary effluent at 5, 15, and 60 minutes of reperfusion. The oxidative stress in the hearts was assessed by estimating malondialdehyde (MDA). The effects of treatments on endogenous antioxidant enzymes were assessed by measuring superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). RESULTS: There was a more significant decrease in the levels of LDH, CPK, CK-MB, and MDA as well as increase in the levels of SOD, CAT and GPx in groups that had received combined treatment in comparison to VA or losartan alone. CONCLUSIONS: It may be concluded that combination of losartan with higher dose of VA decreases ischemic markers and lipid peroxidation and augments endogenous antioxidant and hence, protects myocardium against I/R-induced oxidative stress injuries.