Cortical control of neurally-mediated arrhythmogenic properties of desacetyl lanatoside C: the role of the posterior hypothalamus.

Functional ablation of the cerebral cortex by cortical spreading depression (CSD) significantly increased the dose of desacetyl lanatoside C required to induce A-V block and ventricular fibrillation. To examine the role of the posterior hypothalamus in the increased resistance of decorticated rats to arrhythmia induced by toxic doses of desacetyl lanatoside C, four groups of animals were injected with this drug: group 1 rats had a craniotomy; group 2 rats had a craniotomy and functional decortication; group 3 rats had a craniotomy and a hypothalamic lesion; and group 4 rats had a craniotomy, hypothalamic lesion and functional decortication. The dose of drug required to induce A-V block and ventricular fibrillation was significantly less in group 1, than in groups 2,3 and 4, and there was no statistically significant difference between these last three groups. These results are consistent with the hypothesis that the increased resistance to arrhythmia induced by desacetyl lanatoside C in decorticated rats is mediated by the posterior hypothalamus.