Koichi Sato
Juntendo University
22 Papers
416 Citations
Koichi Sato is an academic researcher from Juntendo University. The author has contributed to research in topics: Pulmonary hypertension & Nitric oxide synthase. The author has an hindex of 17, co-authored 22 publications. Previous affiliations of Koichi Sato include Anschutz Medical Campus.
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Papers
High incidence of aspiration pneumonia in community- and hospital-acquired pneumonia in hospitalized patients: a multicenter, prospective study in Japan.
Shinji Teramoto,Yoshinosuke Fukuchi,Hidetada Sasaki,Koichi Sato,Kiyohisa Sekizawa,Takeshi Matsuse +5 more
TL;DR: Although the statement that plain vitamin D is the treatment of choice for vitamin D deficiency is agreed, there is no high-level evidence of which vitamin D metabolites are safer and faster in normalizing sHPTH, and more importantly, the optimal dose of vitamin D3 capable of normalizing rapidly sHP TH is still being discussed and has not been established.
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The pulmonary circulation of homozygous or heterozygous eNOS-null mice is hyperresponsive to mild hypoxia
Karen A. Fagan,Brian Fouty,Robert C. Tyler,Kenneth G. Morris,Lisa K. Hepler,Koichi Sato,Timothy D. LeCras,Steven H. Abman,Howard D. Weinberger,Paul L. Huang,Ivan F. McMurtry,David M. Rodman +11 more
TL;DR: It is concluded that eNOS-derived NO is an important modulator of the pulmonary vascular response to chronic hypoxia and that more than 50% of eN OS expression is required to maintain normal pulmonary vascular tone.
Relative contributions of endothelial, inducible, and neuronal NOS to tone in the murine pulmonary circulation.
Karen A. Fagan,Robert C. Tyler,Koichi Sato,Brian Fouty,Kenneth G. Morris,Paul L. Huang,Ivan F. McMurtry,David M. Rodman +7 more
TL;DR: It is concluded that in the normal murine pulmonary circulation nNOS does not modulate tone, eNOS-derived nitric oxide is the principle mediator of endothelium-dependent vasodilation in the pulmonary circulation, and both eN OS and iNOS play a role in modulating basal tone chronically.
164
Effects of separate and combined ETA and ETB blockade on ET-1-induced constriction in perfused rat lungs.
TL;DR: Results suggest that in the isolated perfused rat lung, ET-1-induced vasoconstriction is mediated by both ETA and ETB receptors, whereas ET- 1-induced transient vasodilation is mediated exclusively by the ETB receptor.
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Mechanism of hypoxic pulmonary vasoconstriction involves ET(A) receptor-mediated inhibition of K(ATP) channel.
TL;DR: It is suggested that ET-1 contributes to HPV in both isolated lungs and intact animals through ET(A) receptor-mediated suppression of K(ATP)-channel activity.
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