Hypoxemia and blunted hypoxic ventilatory responses in mice lacking heme oxygenase-2

Tetsuya Adachi, Kazunobu Ishikawa, Wataru Hida, Hayato Matsumoto, Takayuki Masuda, Fumiko Date, Kazuhiro Ogawa, Kazuhisa Takeda, Kazumichi Furuyama, Yongzhao Zhang, Tomomi Kitamuro, Hiromasa Ogawa, Yukio Maruyama, Shigeki Shibahara

研究成果: Article査読

70 被引用数 (Scopus)

抄録

Heme oxygenase (HO) catalyzes physiological heme degradation and consists of two structurally related isozymes, HO-1 and HO-2. Here we show that HO-2-deficient (HO-2-/-) mice exhibit hypoxemia and hypertrophy of the pulmonary venous myocardium associated with increased expression of HO-1. The hypertrophied venous myocardium may reflect adaptation to persistent hypoxemia. HO-2-/- mice also show attenuated ventilatory responses to hypoxia (10% O2) with normal responses to hypercapnia (10% CO 2), suggesting the impaired oxygen sensing. Importantly, HO-2 -/- mice exhibit normal breathing patterns with normal arterial CO2 tension and retain the intact alveolar architecture, thereby excluding hypoventilation and shunting as causes of hypoxemia. Instead, ventilation-perfusion mismatch is a likely cause of hypoxemia, which may be due to partial impairment of the lung chemoreception probably at pulmonary artery smooth muscle cells. We therefore propose that HO-2 is involved in oxygen sensing and responsible for the ventilation-perfusion matching that optimizes oxygenation of pulmonary blood.

本文言語English
ページ(範囲)514-522
ページ数9
ジャーナルBiochemical and biophysical research communications
320
2
DOI
出版ステータスPublished - 2004 7 23

ASJC Scopus subject areas

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学

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