A lignocaine infusion worsens the leukoencephalopathy due to a carbon monoxide exposure in sheep.

Poisoning by carbon monoxide (CO) is common and conventional treatment of affected people is frequently unsuccessful. Lignocaine was identified as a potential therapy in this context because of the benefit shown for it in other brain injuries for which the received toxic mechanisms are similar. Twelve Romney ewes were exposed to 1% CO for 120 min were then infused intravenously with either lignocaine (N=6) or saline for 72 h, and were killed 5 days after the exposure for histological and immunohistochemical examination. This dose of CO was narcotic and caused white matter brain infarcts, with associated glial cell activation, axonal dysfunction and induction of both neuronal and glial haeme oxygenase and nitric oxide synthetase. The frequency of the white matter infarcts was significantly greater in the lignocaine-treated group. The mechanism of this adverse interaction is neither established here nor is it deducible from other published data; alternative antidotes to CO clearly need to be tested.