BACKGROUND: Recent studies have shown that improved myocardial salvage after heat-shock pretreatment correlates with the amount of induced cardiac heat-shock protein (HSP)72. However, heat shock also induces myocardial catalase activity, potentially reducing free radical-mediated ischemic injury. The aim of the present study was to determine whether catalase inhibition with 3-amino-1,2,4-triazole (3-AT) abolishes the reduction of infarct size conferred by heat-shock treatment in rats. METHODS AND RESULTS: Myocardial catalase activity was measured in both heat-shocked and control rats 60 minutes after either 3-AT (1000 mg/kg IV) or saline infusion. In separate experiments, heat-shocked and control rats were treated with 3-AT or saline 60 minutes before being subjected to 35 minutes of left coronary artery occlusion and 120 minutes of reperfusion. Infarct size was determined by dual perfusion with triphenyltetrazolium chloride and phthalocyanine blue dye. Heat-shock treatment significantly increased myocardial catalase compared with control animals (180.5 +/- 4.8, n = 6, versus 86.2 +/- 14.7, n = 5, units/g wet wt; P < .05). Treatment with 3-AT significantly reduced myocardial catalase activity in both heat-shocked and control animals (29.6 +/- 5.7, n = 5, and 36.4 +/- 15.3, n = 6, respectively). Heat-shock treatment significantly reduced infarct size in rats that were both treated and untreated with 3-AT compared with respective control groups (22.5 +/- 3.7%, n = 26, 28.2 +/- 4.0%, n = 22, 52.0 +/- 3.0%, n = 23, and 48.6 +/- 3.2%, n = 26, respectively; P < .0001 for both heat-shocked groups versus both control groups; infarct mass/risk area mass x 100). CONCLUSIONS: Catalase inhibition with 3-AT does not abolish the reduction of infarct size in heat-shocked rats.
BACKGROUND: Recent studies have shown that improved myocardial salvage after heat-shock pretreatment correlates with the amount of induced cardiac heat-shock protein (HSP)72. However, heat shock also induces myocardial catalase activity, potentially reducing free radical-mediated ischemic injury. The aim of the present study was to determine whether catalase inhibition with 3-amino-1,2,4-triazole (3-AT) abolishes the reduction of infarct size conferred by heat-shock treatment in rats. METHODS AND RESULTS: Myocardial catalase activity was measured in both heat-shocked and control rats 60 minutes after either 3-AT (1000 mg/kg IV) or saline infusion. In separate experiments, heat-shocked and control rats were treated with 3-AT or saline 60 minutes before being subjected to 35 minutes of left coronary artery occlusion and 120 minutes of reperfusion. Infarct size was determined by dual perfusion with triphenyltetrazolium chloride and phthalocyanine blue dye. Heat-shock treatment significantly increased myocardial catalase compared with control animals (180.5 +/- 4.8, n = 6, versus 86.2 +/- 14.7, n = 5, units/g wet wt; P < .05). Treatment with 3-AT significantly reduced myocardial catalase activity in both heat-shocked and control animals (29.6 +/- 5.7, n = 5, and 36.4 +/- 15.3, n = 6, respectively). Heat-shock treatment significantly reduced infarct size in rats that were both treated and untreated with 3-AT compared with respective control groups (22.5 +/- 3.7%, n = 26, 28.2 +/- 4.0%, n = 22, 52.0 +/- 3.0%, n = 23, and 48.6 +/- 3.2%, n = 26, respectively; P < .0001 for both heat-shocked groups versus both control groups; infarct mass/risk area mass x 100). CONCLUSIONS:Catalase inhibition with 3-AT does not abolish the reduction of infarct size in heat-shocked rats.
Authors: Karl D Pendergrass; Susan T Varghese; Kathryn Maiellaro-Rafferty; Milton E Brown; W Robert Taylor; Michael E Davis Journal: Circ Heart Fail Date: 2010-10-22 Impact factor: 8.790
Authors: A E Bielawska; J P Shapiro; L Jiang; H S Melkonyan; C Piot; C L Wolfe; L D Tomei; Y A Hannun; S R Umansky Journal: Am J Pathol Date: 1997-11 Impact factor: 4.307