Epinephrine-Induced Arrhythmias: Effect of Exogenous Prostaglandins and Prostaglandin Synthesis Inhibition during Halothane-O2 Anesthesia in the Dog

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Abstract

Prostaglandins (PG) modify sympathetic and parasympathetic neurotransmission and have antiarrhythmic properties. Inhibitors of PG synthesis sensitize the heart to certain experimentally induced arrhythmias. This study examined the arrhythmogenic dose (AD) of epinephrine n dogs during halothane-O2 anesthesia as modified by the infusion of PG and by treatment with an inhibitor of PG synthesis.

Dogs were anesthetized with 1.25 MAC halothane. The AD of epinephrine was established by a series of 3-minute epinephrine infusions at 10-minute intervals. The AD of epinephrine was then redetermined during infusions of PG (PGE1—1 μg/kg/min and PGF2 alpha—1 μg/ kg/min), after indomethacin, 3 mg/kg, and after aminophylline, 10 mg/kg. The AD remained unchanged from control during both of the PG infusions and following indomethacin. Only Following aminophylline did the AD decrease significantly.

Our study suggests that pretreatment of surgical patients with nonsteroidal antiinflammatory drugs which inhibit PG synthesis does not increase the likelihood of ventricular arrhythmias during halothane-O2 anesthesia.

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