Influences of Splanchnic Blood Flow on Epinephrine-Induced Hyperkalemia 1

Abstract

Summary

The effect of beta blockade on epinephrine induced hepatic K⁺ mobilization was examined by measuring hepatic arteriovenous K⁺ differences and splanchnic blood flow following epinephrine injections before and after administration of propranolol.

The results demonstrated that alterations in splanchnic blood flow significantly modify the epinephrine-induced systemic hyperkalemic response either by reducing liver perfusion during the period of hepatic K⁺ efflux or by diminishing the amount of epinephrine delivered to that organ. It was evident that using systemic arterial K⁺ concentrations as an index of hepatic K⁺ movements is inadvisable. To assess adequately the ability of an adrenergic agonist to mobilize hepatic K⁺, or the ability of an antagonist to disrupt that process, measurements of hepatic effluent K⁺ and splanchnic blood flow must be made. The present experiments do not support the contention that the adrenergically-induced movement of K⁺ into or out of the liver depends upon the activation of beta receptors.