Acute dimethyl sulphoxide therapy in experimental brain oedema, effect of dose and concentration on brain water and electrolyte content

Abstract

Albino rabbits with experimental brain oedema produced by a combined left hemisphere cryogenic injury and a metabolic insult by a 6-aminonicotinamide (6-ANA) were administered intravenous dimethyl sulphoxide (DMSO) in varying concentrations and doses in the following manner: Subgroup A (concentration response) received 1.0 g/kg bolus of a 10, 20, 30, or 40% solution. Subgroup B (dose response) received as a 20% solution a 1.0 g/kg bolus, 1.5 g/kg bolus, or 2.0 g/kg infusion. One hour following administration of the agent, the animals were killed, their brains rapidly removed by craniectomy and brain water, sodium and potassium measured. Significant decreases in brain sodium and water content in the right hemisphere were noted in both subgroups A (p less than 0.05) and B (p less than 0.005) and in the left hemisphere in subgroup B only (p less than 0.005). There is an apparent effect on brain oedema by a DMSO mediated sodium dependent water mobilization.

Suspected venous air embolism in three horses

“…Additional therapy administered to Case 1 included dimethyl sulphoxide, magnesium sulphate, thiamin, aspirin (as anticoagulant) and vitamin E for its antioxidant effects in brain mitochondria (Navarro and Boveris 2008). The use of dimethyl sulphoxide has been advocated for the treatment of cerebral oedema (Tsuruda et al 1983) and for the hydroxyl radical scavenging properties of this compound (Santos et al 2003). Administration of magnesium sulphate was aimed at elevation of seizure threshold (Hallak 1998) and neuroprotective properties of the drug in experimental models of cerebral ischaemia (Muir 1998).…”

Pharmacokinetics, disposition, and plasma concentrations of dimethyl sulfoxide (DMSO) in the horse following topical, oral, and intravenous administration

“…Studies conducted in a number of species suggested that i.v. administration was effective in reducing intracranial pressure and volume (Camp, James, & Werner, 1981;Ikeda & Long, 1990;Kulah, Akar, & Baykut, 1990;Rucker, Lumb, & Scott, 1981;Tsuruda, James, Werner, Camp, & Rasmussen, 1983;Tung, James, Drummond, & Moore, 1986). Part of its therapeutic efficacy may be based on its ability to scavenge oxygen-free radicals, which have been implicated in induced tissue damages when given before, during, or several hours after tissue insult (Ali, 2001).…”