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Amelioration of ischemia- and reperfusion-induced myocardial injury by the selective estrogen receptor modulator, raloxifene, in the canine heart

Hisakazu Ogita, MD^*, Koichi Node, MD^*,*, Hiroshi Asanuma, MD^*, Shoji Sanada, MD^*, Yulin Liao, MD^*, Seiji Takashima, MD^*, Masanori Asakura, MD^*, Hidezo Mori, MD, Yoshiro Shinozaki, MD, Masatsugu Hori, MD, FACC^* and Masafumi Kitakaze, MD, FACC

^* Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan
Department of Physiological Science, Tokai University School of Medicine, Isehara, Japan
Cardiovascular Division of Medicine, National Cardiovascular Center, Suita, Japan
Department of Cardiac Physiology, National Cardiovascular Center, Suita, Japan

View larger version (25K): [in a new window]   Figure 1 The changes in heart rate and mean arterial pressure during the experiment in each group are shown. No difference in heart rate or mean arterial pressure was observed throughout the experiment between the groups. CTX = charybdotoxin; l-NAME = NG-nitro-l-arginine methyl ester.

View larger version (16K): [in a new window]   Figure 2 Infarct size as a percentage of the area at risk in the various experimental groups. Data from individual animals and mean ± SE values are shown. *p < 0.01 vs. control group. p < 0.05 vs. raloxifene (5 µg/kg per min) group. p < 0.05 vs. control group. p < 0.01 vs. raloxifene (5 µg/kg per min) group. CTX = charybdotoxin; l-NAME = NG-nitro-l-arginine methyl ester.

View larger version (37K): [in a new window]   Figure 3 (A) Increases in p38 MAP kinase, JNK, and ERK activities in each group, compared with the "no ischemia" group, are shown (mean ± SE, n = 3 in each group). These MAP kinases were all activated during ischemia, whereas only p38 MAP kinase was inhibited by infusion of raloxifene into the coronary artery. The activities of the three kinases have been normalized to their total content. *p < 0.01 vs. group with no ischemia. p < 0.05 vs. group with ischemia. p < 0.05 vs. group with raloxifene pretreatment without inhibitors (e.g., L-NAME and CTX). (B) Representative results in each kinase are shown.