Vision, RetinaMagnesium plus mexiletine inhibit energy usage and protect retinas against ischemiaMaynard, Kenneth I.1,3; Quiñones-Hinojosa, Alfredo1; Ogilvy, Christopher S.2Author Information 1Neurophysiology Laboratory, Edwards 414, Neurosurgical Service, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA 2Cerebrovascular Surgery, Edwards 414, Neurosurgical Service, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA 3Corresponding Author: Kenneth I. Maynard ACKNOWLEDGEMENTS: The authors wish to thank Drs M. Flint Beal and A. Ames III for constructive criticism of the manuscript, Junaid Malek for technical assistance and Boehringer Ingelheim Pharmaceutical Inc. for providing mexiletine. K.I.M. is an American Heart Association, Minority Scientist Development Awardee. A.Q. was a Howard Hughes Medical Institute, Medical Student Research Training Fellow. C.S.O. is the recipient of a grant from the National Institutes of Health (NINDS, NS01732). Received 26 August 1998; accepted 30 September 1998 NeuroReport: December 21st, 1998 - Volume 9 - Issue 18 - p 4141-4144 Buy Abstract WE determined whether exogenous Mg2+ and/or mexiletine (Mex), which are reported to be neuroprotective agents, reduced neuronal energy requirements and protected against ischemia, using isolated rabbit retinas. Under non-ischemic conditions, Mex (30 μM) and the combination of Mg2+ (1 mM) plus Mex (30 μM) significantly reduced glucose utilization, by 19% and 31%, respectively. The combination of Mg2+ plus Mex, but not either agent alone, significantly reduced lactate production (by 18% p < 0.05). When added during 2 h of ischemia (simulated by the reduction of oxygen from 95% to 15% and of glucose from mM to 1 mM), Mg2+ plus Mex improved the recovery of glucose utilization (p < 0.01), lactate production (p < 0.05) and neuronal function (p < 0.05) for 3 h following return to control (post-ischemia/recovery) conditions. Thus reducing energy demands by blocking functions during temporary ischemia, protects neurons from irreversible functional damage © 1998 Lippincott Williams & Wilkins, Inc.