The effect of cytochalasin B on cerebral glucose transport and metabolism was investigated in 19 isolated perfused dog brain preparations. Cytochalasin B is a potent, non-competitive inhibitor of glucose transport at the blood-brain interface. Both glucose transport into (Ki = 6.6 ± 1.9 μM) and out of the capillary endothelial cell are inhibited. The inhibition is readily reversible by perfusion with blood containing no cytochalasin B. After 2 min of exposure to 30 μM cytochalasin B, the cerebral oxygen consumption decreased by 31% probably due to decreased availability of glucose for oxidative metabolism. About one-half of the cytochalasin B that is dissolved in blood is bound to erythrocytes and other blood components while the remainder is free.
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The authors gratefully acknowledge the technical assistance of Mr. Paul Con-way, Mr. Wilbert Heiman, Mr. Bruce Levin, Mr. Alton Mitmoen, Mr. Bill Patter-son, Mr. Mark Saffitz and Miss Karla Raab. This investigation was supported by grant NS 05961 from the National Institute of Neurological Diseases and Stroke. A.L.B. gratefully acknowledges the receipt of a Medical Scientist Tram-ing Award. R.W.H. gratefully acknowledges a travel grant from the Wellcome Trust.
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