[The effect of beta-adrenergic blockade on the plasma potassium elevation induced by acute respiratory acidosis during halothane or fentanyl anesthesia].

: The effect of beta-adrenergic blockade on the plasma potassium elevation induced by acute respiratory acidosis (CO2 inhalation) was studied in adult mongrel dogs during halothane or fentanyl anesthesia. Twenty-two dogs were divided into 4 groups: halothane-control (HC, n = 15), halothane-beta-blockade (H beta, n = 8), fentanyl-control (FC, n = 15) and fentanyl-beta-blockade (F beta, n = 10). Beta-blockade was achieved by continuous infusion of propranolol. The maximum levels of plasma potassium after 14% CO2 inhalation were 5.0 +/- 0.7 mM (mean +/- SD) in HC, 6.1 +/- 0.8 mM in H beta, 4.3 +/- 0.4 mM in FC and 4.8 +/- 0.5 mM in F beta. With halothane anesthesia more prominent elevation was observed in the beta-blockade group (P < 0.05), but with fentanyl anesthesia this elevation was not significantly different between the two groups. In acute respiratory acidosis, pH-induced plasma potassium elevation is suppressed by simultaneously increased catecholamines, especially epinephrine. Beta-adrenergic blockade, therefore, may cause severe hyperkalemia due to inhibition of adrenergic potassium disposal. During fentanyl anesthesia plasma potassium elevation was less marked than during halothane. This indicates that fentanyl has less suppressing action on the secretion of stress hormones, including epinephrine, under similarly stressful conditions as halothane anesthesia.