A subanesthetic concentration of sevoflurane increases regional cerebral blood flow and regional cerebral blood volume and decreases regional mean transit time and regional cerebrovascular resistance in volunteers

Inhaled anesthetics exert metabolically mediated effects on cerebral blood vessels both directly and indirectly. We investigated the effects of a 0.4 minimum alveolar subanesthetic concentration of sevoflurane on regional cer ebral blood flow (rCBF), regional cerebral brood volume (rCBV), regional ce rebrovascular resistance (rCVR), and regional. mean transit time (rMTT) in volunteers by means of contrast-enhanced magnetic resonance imaging perfusi on measurement. Sevoflurane increased rCBF by 16% to 55% (control, 55.03 +/ - 0.33 to 148.83 +/- 1.9 mL . 100 g(-1) . min(-1); sevoflurane, 71.75 +/- 0 .36 to 193.26 +/- 2.14 mL . 100 g(-1) . min(-1)) and rCBV by 7% to 39% (con trol, 4.66 +/- 0.03 to 10.04 +/- 0.12 mL/100 g; sevoflurane, 5.04 +/- 0.03 to 13.6 +/- 0.15 mL/100 g); however, sevoflurane decreased rMTT by 7% to 18 % (control, 3.75 +/- 0.04 to 5.39 +/- 0.04 s; sevoflurane, 3.4 +/- 0.03 to 4.44 +/- 0.03 s) and rCVR by 22% to 36% (control, 0.74 +/- 0.01 to 1.9 +/- 0.2 mm Hg/[mL . 100 g(-1) . min(-1)]; sevoflurane, 0.54 +/- 0.01 to 1.41 +/ - 0.01 mm Hg/[mL . 100 g(-1) . min(-1)]). Interhemispheric differences in r CBF, rCBV, and rCVR were markedly reduced after the administration of sevof lurane. These findings are consistent with the known direct vasodilating ef fect of sevoflurane. The decrease in rMTT further shows that rCBF increases more than does rCBV. Furthermore, we can show that the observed increase i n rCBF during inhalation of sevoflurane is not explained by vasodilation al one.