De Luca B, Cerciello A, Monda M
Neuropharmacology. 1982 Nov;21(11):1211-4. doi: 10.1016/0028-3908(82)90183-6.
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.
皮层扩散性抑制（CSD）对大脑皮层的功能性损伤显著增加了诱发房室传导阻滞和心室颤动所需的去乙酰毛花苷C剂量。为了研究下丘脑后部在去皮质大鼠对大剂量去乙酰毛花苷C诱发心律失常的耐受性增加中所起的作用，将四组动物注射这种药物：第1组大鼠进行了开颅手术；第2组大鼠进行了开颅手术和功能性去皮质；第3组大鼠进行了开颅手术和下丘脑损伤；第4组大鼠进行了开颅手术、下丘脑损伤和功能性去皮质。诱发房室传导阻滞和心室颤动所需的药物剂量在第1组显著低于第2、3和4组，后三组之间无统计学显著差异。这些结果与以下假设一致，即去皮质大鼠对去乙酰毛花苷C诱发心律失常的耐受性增加是由下丘脑后部介导的。
