Impaired hypoxic vasoconstriction in intraacinar microvasculature in hyperoxia-exposed rat lungs

Koichi Suzuki, Katsuhiko Naoki, Hiroyasu Kudo, Kazumi Nishio, Nagato Sato, Takuya Aoki, Yukio Suzuki, Kei Takeshita, Atsushi Miyata, Harukuni Tsumura, Yuki Yamakawa, Kazuhiro Yamaguchi

Research output: Contribution to journalArticle

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Abstract

To assess the effects of exposure of the lung to hyperoxic conditions on reactivity of pulmonary microcirculation to hypoxic stimulation, we measured hypoxia-elicited overall pulmonary pressor changes (HPV) and microvascular diameter changes in intraacinar arterioles, venules, and capillaries in isolated perfused rat lungs exposed to a hyperoxic environment (90% O2). To estimate the importance of vasoactive prostaglandins and nitric oxide (NO) for HPV modification, we examined the roles of constitutive and inducible forms of cyclooxygenase (COX-1 and COX-2) and those of NO synthase (eNOS and iNOS). Indomethacin was used for inhibiting both COX-1 and COX-2, while NS- 398 was used as a selective inhibitor of COX-2. Both eNOS and iNOS were suppressed by L-NAME, whereas iNOS alone was inhibited by aminoguanidine. Microvascular diameter was measured with a real-time confocal laser scanning luminescence microscope. We found that (1) exposure to hyperoxia caused overall HPV and arteriolar constriction to be attenuated; (2) the blunted HPV was restored by L-NAME but not by aminoguanidine, indomethacin, or NS-398; and (3) arteriolar constriction was improved by either L-NAME, aminoguanidine, or indomethacin but only slightly by NS-398. In conclusion, attenuation of overall HPV in hyperoxia-exposed lungs is explicable mainly by excessive NO generated via eNOS, while impaired arteriolar constriction is caused by NO yielded by eNOS and iNOS as well as by vasodilating prostaglandin(S) produced by COX-1.

Original languageEnglish
Pages (from-to)602-609
Number of pages8
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume158
Issue number2
Publication statusPublished - 1998
Externally publishedYes

Fingerprint

Hyperoxia
Microvessels
Vasoconstriction
NG-Nitroarginine Methyl Ester
Lung
Constriction
Indomethacin
Nitric Oxide
montirelin
Prostaglandins
Cyclooxygenase 1
Venules
Cyclooxygenase 2 Inhibitors
Arterioles
Microcirculation
Luminescence
Nitric Oxide Synthase
Lasers
pimagedine
N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Suzuki, K., Naoki, K., Kudo, H., Nishio, K., Sato, N., Aoki, T., ... Yamaguchi, K. (1998). Impaired hypoxic vasoconstriction in intraacinar microvasculature in hyperoxia-exposed rat lungs. American Journal of Respiratory and Critical Care Medicine, 158(2), 602-609.

Impaired hypoxic vasoconstriction in intraacinar microvasculature in hyperoxia-exposed rat lungs. / Suzuki, Koichi; Naoki, Katsuhiko; Kudo, Hiroyasu; Nishio, Kazumi; Sato, Nagato; Aoki, Takuya; Suzuki, Yukio; Takeshita, Kei; Miyata, Atsushi; Tsumura, Harukuni; Yamakawa, Yuki; Yamaguchi, Kazuhiro.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 158, No. 2, 1998, p. 602-609.

Research output: Contribution to journalArticle

Suzuki, K, Naoki, K, Kudo, H, Nishio, K, Sato, N, Aoki, T, Suzuki, Y, Takeshita, K, Miyata, A, Tsumura, H, Yamakawa, Y & Yamaguchi, K 1998, 'Impaired hypoxic vasoconstriction in intraacinar microvasculature in hyperoxia-exposed rat lungs', American Journal of Respiratory and Critical Care Medicine, vol. 158, no. 2, pp. 602-609.
Suzuki, Koichi ; Naoki, Katsuhiko ; Kudo, Hiroyasu ; Nishio, Kazumi ; Sato, Nagato ; Aoki, Takuya ; Suzuki, Yukio ; Takeshita, Kei ; Miyata, Atsushi ; Tsumura, Harukuni ; Yamakawa, Yuki ; Yamaguchi, Kazuhiro. / Impaired hypoxic vasoconstriction in intraacinar microvasculature in hyperoxia-exposed rat lungs. In: American Journal of Respiratory and Critical Care Medicine. 1998 ; Vol. 158, No. 2. pp. 602-609.
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