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NEUROSURGICAL ANESTHESIA

Lidocaine Impairs Vasodilation Mediated by Adenosine Triphosphate-Sensitive K⁺ Channels but Not by Inward Rectifier K⁺ Channels in Rat Cerebral Microvessels

Hiroyuki Kinoshita, MD PhD^*, Katsutoshi Nakahata, MD, Mayuko Dojo, MD^*, Yoshiki Kimoto, MD^*, and Yoshio Hatano, MD PhD^*

*Department of Anesthesiology, Wakayama Medical University; and Department of Anesthesia, Japanese Red Cross Society Wakayama Medical Center, Japan

Address correspondence and reprint requests to Hiroyuki Kinoshita, MD, PhD, Department of Anesthesiology, Wakayama Medical University, 811–1 Kimiidera, Wakayama, Wakayama 641–0012, Japan. Address e-mail to hkinoshi{at}pd5.so-net.ne.jp

Vasodilator effects of adenosine triphosphate (ATP)-sensitive, as well as inward rectifier, K⁺ channel openers have not been well demonstrated in cerebral microvessels. Although lidocaine impairs vasorelaxation via ATP-sensitive K⁺ channels in the rat aorta, the effects of this compound on K⁺ channels in the cerebral circulation have not been shown. We designed the present study to examine whether ATP-sensitive and inward rectifier K⁺ channels contribute to vasodilator responses in cerebral microvessels and whether the vasodilation mediated by these channels is inhibited by lidocaine. Rat brain slices were monitored using a computer-assisted videomicroscopy. Cerebral parenchymal arterioles (diameter, 5–10 µm) were contracted with prostaglandin F₂, and thereafter potassium chloride (KCl), levcromakalim, or sodium nitroprusside was added to the perfusion chamber. Levcromakalim and KCl produced vasodilation of the cerebral parenchymal arterioles, which was abolished by an ATP-sensitive K⁺ channel antagonist, glibenclamide, or an inward rectifier K⁺ channel antagonist, barium chloride, respectively. Lidocaine (10^–5 to 3 x 10^–5 M) inhibited the dilation produced by levcromakalim but not by KCl or sodium nitroprusside. In parenchymal arterioles of the cerebral cortex, lidocaine seems to reduce vasodilation mediated by ATP-sensitive K⁺ channels but not by inward rectifier K⁺ channels.

IMPLICATIONS: In parenchymal arterioles of the rat cerebral cortex, lidocaine impairs vasodilation mediated by adenosine triphosphate (ATP)-sensitive K⁺ channels but not by inward rectifier K⁺ channels. These results indicate that lidocaine may impair vasodilator responses mediated via ATP-sensitive K⁺ channels, resulting in decreased cerebral parenchymal perfusion.

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