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Anesth Analg 2007;104:112-118
© 2007 International Anesthesia Research Society
doi: 10.1213/01.ane.0000251200.14449.4a

ANESTHETIC PHARMACOLOGY

Propofol Increases Pulmonary Vascular Resistance During {alpha}-Adrenoreceptor Activation in Normal and Monocrotaline-Induced Pulmonary Hypertensive Rats

Mitsutaka Edanaga, MD*, Masayasu Nakayama, MD*, Noriaki Kanaya, MD{dagger}, Noritsugu Tohse, MD, PhD*, and Akiyoshi Namiki, MD, PhD*

From the Departments of *Anesthesiology and {dagger}Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.

Address correspondence and reprint requests to Mitsutaka Edanaga, MD, S1, W16, Chuo-ku, Sapporo, Hokkaido, 0608543, Japan. Address e-mail to edanaka{at}sapmed.ac.jp.

BACKGROUND: Using isolated perfused lungs of normal or monocrotaline (MCT: 50 mg/kg)-induced pulmonary hypertensive rats, we tested the hypothesis that the pulmonary vascular effects of propofol depend on activation of the {alpha}-adrenoreceptor.

METHODS: Changes in pulmonary perfusion pressure induced by propofol (10–5 to 10–4 M) were measured with or without phenylephrine (10–6 M) pretreatment. Before phenylephrine administration, we assessed the effects of inhibitors of nitric oxide synthase (N{omega}-nitro-l-arginine methylester: 10–4 M), cyclooxygenase (indomethacin: 10–5 M), and protein kinase C inhibitor, bisindolylmaleimide I (10–6 M) or calphostin C (10–6 M).

RESULTS: Changes in pulmonary perfusion pressure by phenylephrine after pretreatment of nitric oxide synthase inhibitor and indomethacin in normal rats were significant (5 ± 3 and 7 ± 2 mm Hg), whereas that after pretreatment of bisindolylmaleimide I were small in MCT-rats (2 ± 1 mm Hg). Propofol caused pulmonary vasoconstriction after phenylephrine pretreatment both in normal and MCT-treated rats. In normal rats, the propofol-induced increase in pulmonary perfusion pressure after indomethacin pretreatment was slightly smaller than that in the non-pretreated lungs (P < 0.05). In MCT-treated rats, the propofol-induced increases in pulmonary perfusion pressure after both protein kinase C inhibitors were smaller than that in the non-pretreated lungs (P < 0.05).

CONCLUSIONS: Propofol may increase pulmonary vascular resistance during {alpha}-adrenoreceptor activation.






Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2007 by the International Anesthesia Research Society.