scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

Electron Spin Resonance Detection of Hydrogen Peroxide as an Endothelium-Derived Hyperpolarizing Factor in Porcine Coronary Microvessels

TL;DR: ESR evidence is provided that H2O2 is an EDHF in porcine coronary microvessels and bradykinin- or substance P–stimulated intact blood vessels by ESR spectroscopy, which indicates a role for endothelium-derived hyperpolarizing factor in modulating vascular tone.
Journal ArticleDOI

Long-term treatment with eicosapentaenoic acid augments both nitric oxide-mediated and non-nitric oxide-mediated endothelium-dependent forearm vasodilatation in patients with coronary artery disease.

TL;DR: Results indicate that long-term treatment with EPA augments both NO-dependent and non-NO-dependent endothelium-dependent forearm vasodilatation in patients with coronary artery disease, and the beneficial effects of EPA appear to extend to non-no-dependent mechanism(s).
Journal ArticleDOI

Inflammatory stimuli upregulate Rho-kinase in human coronary vascular smooth muscle cells

TL;DR: The results indicate that the expression and function of Rho-kinase are upregulated by inflammatory stimuli in hcVSMC with an involvement of PKC and NF-kappaB both in vitro and in vivo.
Journal ArticleDOI

Intramural delivery of a specific tyrosine kinase inhibitor with biodegradable stent suppresses the restenotic changes of the coronary artery in pigs in vivo

TL;DR: Results indicate that intramural delivery of a specific tyrosine kinase inhibitor with biodegradable stent overcomes the proliferative stimuli caused by balloon injury, the stent itself, and the drug coating on theStent, resulting in the suppression of the restenotic changes of the coronary artery in vivo.