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NEUROSURGICAL ANESTHESIA

L-Arginine and Nitroglycerin Restore Hypercapnia-Induced Cerebral Vasodilation in Rabbits After its Attenuation by Ketamine

Department of Anesthesiology & Critical Care Medicine, Gifu University School of Medicine, Gifu City, Japan

Address correspondence and reprint requests to Hiroki Iida, MD, Department of Anesthesiology & Critical Care Medicine, Gifu University School of Medicine, Gifu City, Gifu 500-8705, Japan. Address e-mail to iida{at}cc.gifu-u.ac.jp

Although it has been reported that ketamine attenuates hypercapnia-induced cerebral vasodilation, the mechanism remains unknown. Because nitric oxide is involved in cerebral CO₂ reactivity, we studied the effects of L-arginine and nitroglycerin on ketamine-mediated attenuation of vascular responses to hypercapnia. Under pentobarbital anesthesia, 16 rabbits underwent closed cranial window preparation. Hypercapnic challenges were repeated after IV saline, ketamine (10 mg/kg, followed by 20 mg · kg^-1 · h^-1), or ketamine plus either L-arginine (150 mg/kg, followed by 100 mg · kg^-1 · h^-1; n = 8) or nitroglycerin (5 µg · kg^-1 · min^-1 infusion; n = 8). Ketamine reduced hypercapnia-induced cerebral vasodilation (1.27%/mm Hg ± 0.45%/mm Hg [saline] versus 0.82%/mm Hg ± 0.53%/mm Hg [ketamine]: P < 0.05), but L-arginine restored reactivity (1.28%/mm Hg ± 0.73%/mm Hg: P < 0.05 versus ketamine), as did nitroglycerin (1.14%/mm Hg ± 0.73%/mm Hg [saline] versus 0.56%/mm Hg ± 0.63%/mm Hg [ketamine]: P < 0.05, and 1.15%/mm Hg ± 0.74%/mm Hg [ketamine plus nitroglycerin]: P < 0.05 versus ketamine). This indicates that ketamine attenuates cerebral CO₂ reactivity, at least in part, via suppression of nitric oxide-cyclic guanosine monophosphate mechanisms in the cerebral vasculature.

IMPLICATIONS: The attenuation of cerebral vasodilation to hypercapnia seen under ketamine anesthesia is reversed by L-arginine or nitroglycerin infusion.

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