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ANESTHETIC PHARMACOLOGY

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

Mitsutaka Edanaga, MD^*, Masayasu Nakayama, MD^*, Noriaki Kanaya, MD, Noritsugu Tohse, MD, PhD^*, and Akiyoshi Namiki, MD, PhD^*

From the Departments of *Anesthesiology and 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 -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-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 -adrenoreceptor activation.