• M P Zalunardo, A Zollinger, D R Spahn, B Seifert, M Radjaipour, K Gautschi, and T Pasch.
• Institute of Anesthesiology, University Hospital Zurich, Switzerland.
• J Clin Anesth. 1997 Mar 1;9(2):143-7.

Study ObjectiveTo investigate the effects of intravenous (IV) versus oral clonidine on alterations of heart rate (HR), mean arterial pressure (MAP), cardiac output (CO), and plasma-catecholamines due to endotracheal intubation.DesignRandomized, double-blind, placebo-controlled study.SettingUniversity hospital surgery operating room.Patients33 ASA physical status I patients were randomly assigned to either receive clonidine 3 micrograms/kg IV immediately prior to anesthesia induction, clonidine 4 micrograms/kg orally 90 minutes prior to anesthesia induction, or placebo.InterventionsInsertion of a 14 G cannula in a large cubital vein for the determination of plasma-catecholamines using local anesthesia. Insertion of a radial artery catheter for measuring blood pressure (BP) using local anesthesia. Transthoracic echocardiography determined CO.Measurements And Main ResultsHeart rate, MAP, CO, and plasma-catecholamine concentrations were measured. Measurements were performed prior to induction, during intubation, and 10 minutes after intubation. During endotracheal intubation, MAP was significantly lower in the IV clonidine group compared with the placebo and the oral clonidine groups. Cardiac output was significantly lower in the IV clonidine group only. In contrast to the placebo group, norepinephrine plasma concentrations did not increase in either clonidine group. Significant alterations of epinephrine plasma concentrations due to intubation were not observed in either group. Hemodynamics after intubation were not impaired by clonidine treatment.ConclusionsIn conclusion, IV clonidine reduced stress response to endotracheal intubation compared with placebo. Oral clonidine at the dose used was less effective in blunting hemodynamic stress response than IV clonidine.

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