Early Restoration of Cocaine-Induced Splanchnic Hypoperfusion in Anesthetized Dogs

Abstract

Although cardiovascular effects of cocaine have been well studied, little is known about its effects on splanchnic perfusion. We studied systemic and regional hemodynamic effects of acute cocaine intoxication in dogs under volatile anesthesia. Mechanically ventilated beagle dogs, randomized at 1.5% halothane (n = 7) or 2.25% sevoflurane (n = 7) anesthesia, received an intravenous bolus of cocaine (12 mg/kg over 5 min) followed by 0.22 mg/kg/min infusion over 30 min. They were observed for 60 min thereafter. Cardiac index (CI), heart rate (HR), mean arterial pressure (MAP), portal blood flow (PBF), gastric PCO2 (gas tonometry), blood gases, and lactate and cocaine levels were assessed. Cocaine bolus promoted significant reductions in CI (∼ 50%), HR (∼ 20%), MAP (∼ 20%), and PBF (∼ 50%), accompanied by increase in systemic and splanchnic oxygen extractions and in gastric mucosal–arterial PCO2 gradient. Those changes were maintained during cocaine infusion and returned to baseline values parallel to plasmatic cocaine clearance. Unlike other shock states, regional parameters, including gastric mucosal–arterial PCO2 gradient, were restored before systemic variables. A possible local vasodilatory effect of volatile agents could play a role in this phenomenon. Cocaine infusion in anesthetized animals promoted marked systemic and regional hemodynamic derangement, which was rapidly reversible with decay of cocaine plasmatic concentration.