Key result
Ethanol ingestion increased forearm blood flow and skin temperature in controls but not in quadriplegics, suggesting peripheral vasodilation is induced by central vasomotor control mechanisms.
Why the study?
Does ethanol ingestion induce peripheral vasodilation via central vasomotor control mechanisms?
Does ethanol ingestion induce peripheral vasodilation via central vasomotor control mechanisms?
Ethanol-induced peripheral vasodilation appears to be mediated by central vasomotor control mechanisms rather than direct peripheral action.
Ethanol vasodilation appears centrally mediated; leaves open confirmation in larger cohorts before informing autonomic management in spinal injury.
The mechanism by which ethanol ingestion causes dermal vasodilation is unclear, but it may result from a direct action on central vascular control mechanisms. Forearm blood flow and peripheral skin temperatures were examined in five quadriplegics (lesions above T7) and five control subjects, before and after the ingestion of ethanol (0.75 ml/kg body wt). The lack of vasomotor efferent function was confirmed in the quadriplegics by the absence of vasodilation in response to radiant heating of the torso. There were no significant changes in peripheral temperatures or forearm blood flow after ethanol in the quadriplegics. The control subjects had a significant increase in forearm blood flow (1.12 +/- 0.2 ml.min-1.100 ml-1) and skin temperature (finger 2.4 +/- 0.4 degrees C, toe 3.4 +/- 0.3 degrees C) after ethanol. These data suggest that ethanol may induce peripheral vasodilation by modulation of central vasomotor control mechanisms.
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Malpas et al. (1990) studied Quadriplegia (n=10). Ethanol vs. Quadriplegics vs control subjects was evaluated on Forearm blood flow and peripheral skin temperatures. Ethanol ingestion increased forearm blood flow and skin temperature in controls but not in quadriplegics, suggesting peripheral vasodilation is induced by central vasomotor control mechanisms.
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