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Am. J. Respir. Crit. Care Med., Volume 158, Number 2, August 1998, 602-609

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, and KAZUHIRO YAMAGUCHI

Department of Medicine, School of Medicine, Keio University, Tokyo; Biomedical Department, Sankei Corporation, Tokyo; and Pharmacology Laboratory, Pharmaceutical Research Laboratories, Taisho Pharmaceutical Company, Ohmiya, Saitama, Japan

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.




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Copyright © 1998 American Thoracic Society