Seiji Matsuhisa
Kansai Medical University
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Featured researches published by Seiji Matsuhisa.
American Journal of Physiology-heart and Circulatory Physiology | 2008
Seiji Matsuhisa; Hajime Otani; Toru Okazaki; Koji Yamashita; Yuzo Akita; Daisuke Sato; Akira Moriguchi; Hiroji Imamura; Toshiji Iwasaka
Oxidative stress is involved in the tolerance to ischemia-reperfusion (I/R) injury. Because angiotensin II type 1 receptor blockers (ARBs) inhibit oxidative stress, there is concern that ARBs abolish the tolerance to I/R injury. Dahl salt-sensitive (DS) hypertensive and salt-resistant (DR) normotensive rats received an antioxidant, 2-mercaptopropionylglycine (MPG), or an ARB, losartan, for 7 days. Losartan and MPG significantly inhibited oxidative stress as determined by tissue malondialdehyde + 4-hydroxynoneal and increased expression of inducible nitric oxide synthase (iNOS) in the DS rat heart. However, losartan but not MPG activated endothelial nitric oxide synthase (eNOS) as assessed by phosphorylation of eNOS on Ser1177. Infarct size after 30-min left coronary artery occlusion followed by 2-h reperfusion was comparable between DS and DR rat hearts. Although MPG and losartan had no effect on infarct size in the DR rat heart, MPG but not losartan significantly increased infarct size in the DS rat heart. A selective iNOS inhibitor, 1400W, increased infarct size in the DS rat heart, but it had no effect on infarct size in the losartan-treated DS rat heart. However, a nonselective NOS inhibitor, Nomega-nitro-l-arginine methyl ester, increased infarct size in the losartan-treated DS rat heart. These results suggest that losartan preserves the tolerance to I/R injury by activating eNOS despite elimination of redox-sensitive upregulation of iNOS and iNOS-dependent cardioprotection in the DS rat heart.
Antioxidants & Redox Signaling | 2008
Seiji Matsuhisa; Hajime Otani; Toru Okazaki; Koji Yamashita; Yuzo Akita; Daisuke Sato; Akira Moriguchi; Toshiji Iwasaka
Oxidative stress mediated by activation of angiotensin II type-1 receptor (AT(1)R) plays a crucial role in the progression of heart failure. We investigated the effect of N-acetylcysteine (NAC) and an AT(1)R blocker on oxidative stress and left ventricular (LV) remodeling in BIO14.6 cardiomyopathy hamsters. The cardiomyopathy hamsters were treated with NAC or the AT(1)R blocker losartan for 20 weeks. Although NAC and losartan inhibited oxidative stress and upregulation of iNOS in the cardiomyopathy hamster heart, only losartan inhibited LV chamber dilation, myocardial fibrosis, and LV dysfunction in the cardiomyopathy hamster. Co-treatment with NAC abolished the protective effect of losartan against LV remodeling associated with inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt and eNOS activation. An iNOS inhibitor 1400W or a nonselective NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) exacerbated LV remodeling in the cardiomyopathy hamster. However, L-NAME but not 1400W abrogated losartan-mediated inhibition of LV remodeling. These results suggest that redox-sensitive upregulation of iNOS plays a crucial role in preventing LV remodeling in the BIO14.6 cardiomyopathy hamster. Losartan inhibits LV remodeling by switching the cardioprotective mechanism from iNOS- to eNOS-dependence, but NAC abolishes the protective effect of losartan by inhibiting redox-sensitive activation of PI3K/Akt and eNOS in the cardiomyopathy hamster.
American Heart Journal | 2016
Hiroshi Ueda; Atsumichi Kido; Seiji Matsuhisa; Koichiro Asawa; Naohiro Yoshida; Mitsuru Tsujimoto; Yasushi Sasaki; Yukiko Kuga; Masaki Yamasaki; Kazuya Ueda; Shoichi Shinohara; Yasunori Nishida
BACKGROUND Patients with established coronary artery disease are at increased risk for future ischemic events and require secondary prevention for systemic vascular disease. We performed a randomized clinical trial to evaluate the impact of cilostazol on cardiovascular and cerebrovascular disease in patients undergoing percutaneous coronary intervention. METHODS A total of 514 patients who had undergone coronary stent implantation >6 months previously and were thought to no longer need dual antiplatelet therapy with aspirin and a thienopyridine were randomly assigned to receive aspirin plus cilostazol therapy or aspirin therapy alone after discontinuation of thienopyridine therapy. The primary efficacy end point was a composite of all-cause death, myocardial infarction, stroke, or cardiovascular or cerebrovascular revascularization at 2 years after randomization. The main safety end point was major or minor bleeding, according to the Thrombolysis in Myocardial Infarction bleeding definition. RESULTS At 2 years, follow-up clinical data were available for 98.1% of patients. The primary efficacy end point occurred in 13.9% of the aspirin plus cilostazol group versus 22.1% of the aspirin-only group (hazard ratio 0.61, 95% CI 0.40-0.93, P = .021). The rate of major or minor bleeding was not significantly different between the aspirin plus cilostazol and aspirin-only groups (1.6% and 4.0%, respectively, hazard ratio 0.40, 95% CI 0.13-1.28, P = .12). CONCLUSIONS In patients who underwent coronary stent implantation, the addition of cilostazol to aspirin therapy was associated with lower rates of cardiovascular and cerebrovascular events at 2 years compared with aspirin monotherapy.
Cardiovascular Research | 2006
Shiori Kyoi; Hajime Otani; Seiji Matsuhisa; Yuzo Akita; Kimiko Tatsumi; Chiharu Enoki; Hiroyoshi Fujiwara; Hiroji Imamura; Hiroshi Kamihata; Toshiji Iwasaka
American Journal of Physiology-heart and Circulatory Physiology | 2007
Yuzo Akita; Hajime Otani; Seiji Matsuhisa; Shiori Kyoi; Chiharu Enoki; Reiji Hattori; Hiroji Imamura; Hiroshi Kamihata; Yutaka Kimura; Toshiji Iwasaka
Circulation | 2006
Hajime Otani; Seiji Matsuhisa; Yuzo Akita; Shiori Kyoi; Chiharu Enoki; Kimiko Tatsumi; Hiroyoshi Fujiwara; Reiji Hattori; Hiroji Imamura; Toshiji Iwasaka
Cardiovascular Research | 2006
Shiori Kyoi; Hajime Otani; Ayako Hamano; Seiji Matsuhisa; Yuzo Akita; Hiroyoshi Fujiwara; Reiji Hattori; Hiroji Imamura; Hiroshi Kamihata; Toshiji Iwasaka
Antioxidants & Redox Signaling | 2006
Shiori Kyoi; Hajime Otani; Seiji Matsuhisa; Yuzo Akita; Chiharu Enoki; Kimiko Tatsumi; Reiji Hattori; Hiroji Imamura; Hiroshi Kamihata; Toshiji Iwasaka
International Journal of Cardiology | 2006
Koichi Yamada; Hisako Tsuji; Satoshi Tokunaga; Koji Kurimoto; Hirofumi Maeba; Seiji Matsuhisa; Norihito Inami; Toshiji Iwasaka
Journal of the American College of Cardiology | 2013
Hiroshi Ueda; Kojiro Yoshimura; Atsumichi Kido; Kenji Natsuyama; Seiji Matsuhisa; Koichiro Asawa; Naohiro Yoshida; Kazushige Yamaguchi; Yasushi Sasaki; Yukiko Kuga; Masahiro Yamasaki; Kazuya Ueda; Yasunori Nishida