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Halothane is commonly viewed as a more potent cerebral vasodilator than isoflurane. It was speculated that the lesser vasodilation caused by isoflurane might be the result of the greater reduction in cerebral metabolic rate (CMR) that it causes, and that the relative vasodilating potencies of halothane and isoflurane would be similar if the two agents were administered in a situation that precluded volatile-agent-induced depression of CMR. To test this hypothesis, cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMR01) were measured in two groups of rabbits before and after the administration of 0.75 MAC halothane or isoflurane. One group received a background anesthetic of morphine and N2O, which resulted in an initial CMR01 of 3.21 ± 0.17 (SEM) ml · 100 g−1 · min−1; second group received a background anesthetic of high-dose pentobarbital, which resulted in an initial CMR01 of 1.76 ± 0.16 ml · 100 g−1 · min−1. In rabbits receiving a background of morphine sulfate/ N2O, halothane resulted in a significantly greater CBF (65 ± 10 ml · 100 g−1 · min−1) than did isoflurane (40 ± 5 ml · 100 g−1 · min−1). Both agents caused a reduction in CMRO1, but CMRO1 was significantly less during isoflurane administration. By contrast, with a background of pentobarbital anesthesia, CBF increased by significant and similar amounts with both halothane and isoflurane. With halothane, CBF increased from 22 ± 2 ml · 100 g−1 · min−1 in the control state to 39 ± 3, and with isoflurane from 24 ± 2 to 38 ± 2 ml · 100 g−1 · min−1. CMR01 was not depressed further by either halothane or isoflurane. These results suggest that the relative effects of halothane and isoflurane on CBF are dependent on the CMR present prior to their administration. When the preexistent CMR is not markedly depressed, isoflurane decreases CMR and causes less cerebral vasodilation than does halothane. When initial CMR is depressed, halothane and isoflurane have similar vasodilating potencies.