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Visualisation of changes in regional cerebral blood flow (rCBF) produced by ketamine using long TE gradient-echo sequences: preliminary results.

N G Burdett, D K Menon, T A Carpenter, J G Jones, L D Hall

Magnetic resonance imaging 1995 DOI: 10.1016/0730-725x(95)00010-e (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental animal study Peer reviewed
Population Rats anaesthetised with nitrous oxide supplemented with halothane or fentanyl/fluanisone/midazolam
Interventions Ketamine halothane fentanyl/fluanisone/midazolam
Dose low dose (single bolus or low dose infusion)
Topics Esketamine Ketamine
Key findings Low-dose ketamine produced a 10-14% increase in functional MRI signal intensity in the hippocampus, cerebral cortex, and olfactory lobe of rats under fentanyl/fluanisone/midazolam anaesthesia, indicating increased regional cerebral blood flow. This increase was significantly reduced in rats given halothane, which the authors suggest may reflect a halothane effect on ketamine-induced changes similar to its attenuation of dizocilpine effects.

Abstract

Autoradiographic studies have shown that low dose ketamine produces increases in regional glucose utilisation and blood flow in the hippocampus, cerebral cortex, and olfactory lobe in the rat brain, probably due to antagonism at the NMDA receptor. Functional MRI using deoxyhaemoglobin contrast can be used to study changes in regional cerebral blood flow (rCBF). Long TE gradient-echo sequences were used to study changes in rCBF produced by low dose ketamine in rats anaesthetised with nitrous oxide, supplemented with either halothane (HAL) or fentanyl/fluanisone/midazolam (FFM) combination. Images from rats in the FFM group showed a 10-14% increase in signal intensity in the hippocampus, cerebral cortex, and olfactory lobe following either a single bolus or a low dose infusion of ketamine (p < .05). These changes were significantly reduced in the HAL group (p < .005). Halothane is known to attenuate the changes in regional glucose utilisation produced by the noncompetitive NMDA antagonist dizocilpine (MK-801), and its effects on ketamine-induced changes in rCBF seen in this study may be due to a similar effect. The potential use of functional MRI in studying the effect of pharmacological interventions on rCBF is discussed.