Neural factors in digitalis toxicity: protective effect of C-1 spinal cord transection

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Abstract
The autonomic nervous system was shown to play a role in the genesis of cardiac rhythm disturbances. The protective effect of C-1 spinal cord transection, as judged by higher cumulative ouabain dose and myocardial content of glycoside at onset of toxicity, has been cited as evidence implicating the nervous system in digitalis-induced cardiotoxicity. To further define the significance of this apparent protective effect, cats were subjected to C-1 spinal cord section or were left neurally intact and [3H]ouabain was given i.v. (1 .mu.g/kg .cntdot. min) until onset of ventricular tachycardia (VT). The dose to onset of VT and the myocardial content of ouabain were significantly greater in the group with C-1 cord section. In vitro active transport of the K+ analog Rb+ by myocardial samples from neurally intact cats was reduced to 54% of control at onset of VT. Significantly greater transport inhibition, to 30% of the control value, was present at VT in animals with the cord transected at the C-1 level. Active transport of Rb+ at onset of VT was also significantly different between neurally intact animals and animals with C-1 section when the ouabain infusion rate was doubled. Thus, C-1 cord section appears to provide true protection against the emergence of overt digitalis toxicity. This effect cannot be attributed to reduced uptake of the glycoside or to reduced interaction with the putative receptor Na+-K+-ATPase.