Attenuated additional hypocapnic constriction, but not hypercapnic dilation, of spinal pial arterioles during spinal ropivacaine

Ropivacaine constricts spinal vessels. Because the CO2 response of spinal v essels is similar to that of cerebral vessels, we tested to see if hypocapn ia would cause further spinal vasoconstriction during ropivacaine administr ation. In 12 pentobarbital-anesthetized dogs, spinal pial arteriolar diamet er was measured using a closed spinal window preparation. Either ropivacain e solution (0.1%; n = 6) or artificial cerebrospinal fluid (n = 6) was infu sed continuously into the spinal window. After a period of hypocapnia (Paco (2), 20-25 mm Hg) had been induced, inspired CO2 levels were adjusted to pr oduce normocapnia (35-40 mm Hg) followed by hypercapnia (55-60 mm Hg). When the desired Pace, was reached measurements were made of the arteriolar dia meter 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 (al most nonexistent) additional vasoconstriction in the ropivacaine group than in the control group (P < 0.01). The final hypercapnic vasodilation was so mewhat greater during ropivacaine (P < 0.05 versus control group). Topical ropivacaine induced no change in hemodynamic variables. We conclude that hy pocapnia of the magnitude tested did not cause further constriction in spin al vessels during spinal ropivacaine. Implications: During topical applicat ion of the local anesthetic ropivacaine in dogs, hypocapnia (Paco(2) 20-25 mm Hg) induced almost no additional constriction of spinal arterioles, and the hypercapnic vasodilation was maintained. These data suggest that an add itional constriction in spinal vessels is unlikely when hypocapnia occurs d uring spinal ropivacaine.