Effect of Thiopental Induction on Sympathetic Activity
Several recent studies with different anesthetic agents have reported increases in plasma norepinephrine concentration during induction. To determine if induction with intravenous injection of thiopental also is associated with initial sympathetic activation, 24 ASA class I patients were assigned randomly to receive one of the following anesthetics: Group I, thiopental 3 rag/kg, iv, followed by inhalation of 100% oxygen and a continuous intravenous infusion of thiopental 0.2–0.3 mg · kg-1 · min-1; Group II, thiopental 3 mg/kg followed by inhalation of halothane (1.5% end-tidal concentration) in oxygen; and Group III, thiopental 3 mg/kg followed by inhalation of 70% nitrous oxide in oxygen. After thiopental injection, ventilation was controlled to maintain Pco2 near control levels. In Group I, plasma norepinephrine concentration decreased with continued administration of thiopental. This decrease became statistically significant (P < 0.05) 10 min after injection. Plasma epinephrine concentration did not change. For Groups II and III, both plasma norepinephrine and epinephrine concentration did not change. For Groups II and III, the stability of the catecholamine concentrations during induction may have been caused by the circumvention of the second stage of anesthesia, equal depression of both inhibitory and excitatory synapses, or the combined effects of the agents. Regardless of the cause, the use of a modest induction dose of thiopental appears to allow the induction of anesthesia without sympathetic activation. When it is important to prevent sympathetic activation, administering a modest dose of thiopental before the inhalation of halothane or nitrous oxide may be preferable to inducing anesthesia with inhalation agents or narcotics alone.