H
Hiroaki Shimokawa
Researcher at Tohoku University
Publications - 976
Citations - 56856
Hiroaki Shimokawa is an academic researcher from Tohoku University. The author has contributed to research in topics: Heart failure & Endothelium. The author has an hindex of 111, co-authored 949 publications receiving 48822 citations. Previous affiliations of Hiroaki Shimokawa include University of Nebraska Medical Center & Nagoya University.
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Long-term inhibition of Rho-kinase ameliorates diastolic heart failure in hypertensive rats
Shigefumi Fukui,Yoshihiro Fukumoto,Jun Suzuki,Kenya Saji,Jun Nawata,Shunsuke Tawara,Tsuyoshi Shinozaki,Yutaka Kagaya,Hiroaki Shimokawa +8 more
TL;DR: Results indicate that Rho-kinase pathway plays an important role in the pathogenesis of DHF and thus could be an important therapeutic target for the disorder.
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Increased incidence of tachyarrhythmias and heart failure hospitalization in patients with implanted cardiac devices after the great East Japan earthquake disaster.
Makoto Nakano,Masateru Kondo,Yuji Wakayama,Akiko Kawana,Yuhi Hasebe,Mohamed Abdel Shafee,Koji Fukuda,Hiroaki Shimokawa +7 more
TL;DR: The East Japan Earthquake disaster unfavorably affected patients implanted with defibrillators or biventricular pacemakers.
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Effects of combined therapy with a Rho-kinase inhibitor and prostacyclin on monocrotaline-induced pulmonary hypertension in rats.
TL;DR: Combined therapy with a Rho-kinase inhibitor and prostacyclin exerts further beneficial effects on PH, with significantly more improvement in PH, right ventricular hypertrophy, and pulmonary medial thickness without any adverse effects.
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Antianginal effects of hydroxyfasudil, a Rho‐kinase inhibitor, in a canine model of effort angina
TL;DR: Inhibition of Rho‐kinase appears to protect myocardium subjected to pacing‐induced ischaemia through the increase in the regional myocardial blood flow, categorized as a novel type of anti‐anginal drug, without any inotropic or chronotropic effects.
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Overexpression of tumor necrosis factor-α increases production of hydroxyl radical in murine myocardium
Yoji Machida,Toru Kubota,Natsumi Kawamura,Hajime Funakoshi,Tomomi Ide,Hideo Utsumi,Yun You Li,Arthur M. Feldman,Hiroyuki Tsutsui,Hiroaki Shimokawa,Akira Takeshita +10 more
TL;DR: Although cyclophosphamide significantly suppressed the infiltration of inflammatory cells, it did not diminish the production of hydroxyl radical in TG myocardium, indicating that damaged myocytes, but not infiltratinginflammatory cells, may be the source of ROS in TG.