Failure of tetracaine to reverse spinal cord injury in the cat

Malm, D. N.

doi:10.3171/jns.1984.60.6.1269

Cited by 7 publications

(1 citation statement)

References 33 publications

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“…In vivo studies have shown that intravenous lidocaine offered little or at best modest protection against cerebral ischemia (Gelb et aI., 1988;Evans et aI., 1989;Sutherland et aI., 1989;Rasool et aI., 1990;Dutka et at., 1992). The benefit of local anes thetics in spinal cord injury models is likewise mod est (Ford and Maim, 1984;Kobrine et aI., 1984;Haghighi et aI., 1987). However, very few of the many available Na + channel-blocking agents have been tested in vivo, and it appears that the degree of protection versus suppression of excitability in nor mal tissue varies widely from compound to com pound.…”

Section: Antiarrhythmics Protect By Reducing Na + Influxmentioning

confidence: 99%

Protective Effects of Antiarrhythmic Agents against Anoxic Injury in CNS White Matter

Stys

1995

J Cereb Blood Flow Metab

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Irreversible anoxic injury is dependent on extracellular Ca2+ in mammalian CNS white matter, with a large portion of the pathologic Ca2+ influx occurring through reverse Na(+)-Ca2+ exchange, stimulated by increased intracellular [Na+]. This Na+ leak likely occurs via incompletely inactivated voltage-gated Na+ channels. This study reports that clinically used antiarrhythmic compounds, likely by virtue of their Na+ channel-blocking properties, significantly protect CNS white matter from anoxia at concentrations that cause little suppression of the preanoxic response. Rat optic nerves were pretreated with various agents for 60 min, then subjected to 60 min of anoxia in vitro. Functional recovery was measured electrophysiologically as the area under the compound action potential (CAP). Without drug, the CAP areas recovered to a mean of 32 +/- 12% of control after 1 h of reoxygenation. Recoveries using prajmaline 10 microM were 82 +/- 15% (p < 0.0001), and using tocainide 1 mM, 78 +/- 8% (p < 0.0001), with little suppression (< or = 10%) of the preanoxic response. Ajmaline (10-100 microM), disopyramide (10-300 microM) and bupivacaine (10-100 microM) were somewhat less effective, whereas verapamil produced 52 +/- 11% recovery before reduction of the preanoxic CAP was observed at 30 microM. Procainamide (100-300 microM) was ineffective. These results suggest that Na+ channel blockers, including commonly used antiarrhythmic agents, may be effective in protecting central white matter, which is a target for anoxic/ischemic injury in diseases such as stroke and spinal cord injury.

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