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REGIONAL ANESTHESIA AND PAIN MANAGEMENT

Attenuated Additional Hypocapnic Constriction, but Not Hypercapnic Dilation, of Spinal Pial Arterioles During Spinal Ropivacaine

Hiroki Iida, MD^*, Hiroto Ohata, MD^*, Mami Iida, MD, Yukinaga Watanabe, MD^*, Kiyoshi Nagase, MD^*, and Shuji Dohi, MD^*

Departments of *Anesthesiology and Critical Care Medicine and Second Department of Internal Medicine, Gifu University School of Medicine, Gifu City, Gifu, Japan

Address correspondence and reprint requests to Hiroki Iida, MD, Department of Anesthesiology and 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

Ropivacaine constricts spinal vessels. Because the CO₂ response of spinal vessels is similar to that of cerebral vessels, we tested to see if hypocapnia would cause further spinal vasoconstriction during ropivacaine administration. In 12 pentobarbital-anesthetized dogs, spinal pial arteriolar diameter was measured using a closed spinal window preparation. Either ropivacaine solution (0.1%; n = 6) or artificial cerebrospinal fluid (n = 6) was infused continuously into the spinal window. After a period of hypocapnia (PaCO₂, 20–25 mm Hg) had been induced, inspired CO₂ levels were adjusted to produce normocapnia (35–40 mm Hg) followed by hypercapnia (55–60 mm Hg). When the desired PaCO₂ was reached, measurements were made of the arteriolar diameter and physiological variables. During normocapnia, ropivacaine infusion produced a significant constriction of pial arterioles, whereas artificial cerebrospinal fluid caused no change. Hypocapnia induced a much smaller (almost nonexistent) additional vasoconstriction in the ropivacaine group than in the control group (P < 0.01). The final hypercapnic vasodilation was somewhat greater during ropivacaine (P < 0.05 versus control group). Topical ropivacaine induced no change in hemodynamic variables. We conclude that hypocapnia of the magnitude tested did not cause further constriction in spinal vessels during spinal ropivacaine.

Implications: During topical application of the local anesthetic ropivacaine in dogs, hypocapnia (PaCO₂, 20–25 mm Hg) induced almost no additional constriction of spinal arterioles, and the hypercapnic vasodilation was maintained. These data suggest that an additional constriction in spinal vessels is unlikely when hypocapnia occurs during spinal ropivacaine.

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