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Thromboxane A(2) and prostaglandin F-2 alpha mediate inflammatory tachycardia

https://asahikawa-med.repo.nii.ac.jp/records/301
https://asahikawa-med.repo.nii.ac.jp/records/301
d7e8b0c2-dc59-4007-89b5-e8b8c93c54b8
名前 / ファイル ライセンス アクション
377.pdf 377.pdf (1.2 MB)
Item type 学術雑誌論文 / Journal Article_02(1)
公開日 2007-03-22
タイトル
タイトル Thromboxane A(2) and prostaglandin F-2 alpha mediate inflammatory tachycardia
言語 en
言語
言語 eng
資源タイプ
資源タイプ journal article
著者 牛首, 文隆

× 牛首, 文隆

牛首, 文隆

ja-Kana ウシクビ, フミタカ

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Takayama, K

× Takayama, K

Takayama, K

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Yuhki, K

× Yuhki, K

Yuhki, K

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Ono, K

× Ono, K

Ono, K

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Fujino, T

× Fujino, T

Fujino, T

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Hara, A

× Hara, A

Hara, A

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Yamada, T

× Yamada, T

Yamada, T

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Kuriyama, S

× Kuriyama, S

Kuriyama, S

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Karibe, H

× Karibe, H

Karibe, H

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Okada, Y

× Okada, Y

Okada, Y

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Takahata, O

× Takahata, O

Takahata, O

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Taniguchi, T

× Taniguchi, T

Taniguchi, T

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Iijima, T

× Iijima, T

Iijima, T

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Iwasaki, H

× Iwasaki, H

Iwasaki, H

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Narumiya, S

× Narumiya, S

Narumiya, S

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著者 ローマ字
Ushikubi, Fumitaka
書誌情報 NATURE MEDICINE

巻 11, 号 5, p. 562-566, 発行日 2005-05-01
ISSN
収録物識別子タイプ ISSN
収録物識別子 1078-8956
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 10.1038/nm1231
リンクURL
内容記述タイプ Other
内容記述 http://www.nature.com/nm/journal/v11/n5/full/nm1231.html | http://www.nature.com/nm/journal/v11/n5/full/nm1231.html
抄録
内容記述タイプ Abstract
内容記述 Systemic inflammation induces various adaptive responses including tachycardia. Although inflammation-associated tachycardia has been thought to result from increased sympathetic discharge caused by inflammatory signals of the immune system^1, definitive proof has been lacking. Prostanoids-including prostaglandin (PG) D_2, PGE_2, PGF_<2α>, PGI_2, and thromboxane (TX) A_2-exert their actions through specific receptors: DP, EP (EP_1, EP_2, EP_3, EP_4), FP, IP, and TP, respectively^2. Here we have examined the roles of prostanoids in inflammatory tachycardia with the use of mice lacking each of these receptors individually. The TXA_2 analog I-BOP and PGF_<2α> each increased the beating rate of the isolated atrium of wild-type (WT) mice in vitro through interaction with TP and FP, respectively. The cytokine-induced increase in beating rate was markedly inhibited in atria from mice lacking either TP or FP. The tachycardia induced in WT mice by injection of lipopolysaccharide (LPS) was greatly attenuated in TP-/- or FP-/- mice and was completely absent in mice lacking both TP and FP. Propranolol failed to block the LPS-induced increase in heart rate in WT animals. Our results show that inflammatory tachycardia is caused by a direct action on the heart of TXA_2 and PGF_<2α> formed under systemic inflammatory conditions.
注記
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注記 author
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資源タイプ text
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Cite as

牛首, 文隆, Takayama, K, Yuhki, K, Ono, K, Fujino, T, Hara, A, Yamada, T, Kuriyama, S, Karibe, H, Okada, Y, Takahata, O, Taniguchi, T, Iijima, T, Iwasaki, H, Narumiya, S, n.d., Thromboxane A(2) and prostaglandin F-2 alpha mediate inflammatory tachycardia: 562–566 p.

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