In a canine model of hemorrhagic shock, vasoconstriction appears to be mediated by locally released noradrenaline from sympathetic nerve terminals rather than circulating noradrenaline.
Supports local noradrenaline mediation of canine shock vasoconstriction; hypothesis-generating, requires human validation before clinical relevance.
In dogs subjected to hemorrhagic shock, a marked decrease in the noradrenaline content of the sympathetic nerve terminals in the normally innervated spleen is revealed by means of a histochemical fluorescence method. Deprivation of the sympathetic impulse-flow to the tissue immediately before the animals are subjected to shock prevents this depletion. The results support the hypothesis that the vasoconstriction which occurs during shock is due to the effect of noradrenaline released locally in the tissues, and not to circulating noradrenaline.
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Dahlström et al. (1965) studied this question.
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