Effect of clonidine on changes in plasma catecholamine concentrations and oxygen consumption caused by the cold pressor test.

This study was designed to investigate whether clonidine could attenuate the increase in oxygen consumption (VO2), arterial pressure (AP) and plasma catecholamines in response to the cold pressor test (CPT), an intense stimulation of the sympathetic nervous system. Six volunteers were given clonidine (2 micrograms kg-1 and 4 micrograms kg-1) and placebo i.m. in a random, double-blind, cross-over manner. Both clonidine doses decreased plasma catecholamine concentrations (P < 0.01), but only the higher dose of clonidine attenuated the CPT-induced absolute increase in plasma catecholamine concentration compared with the placebo group (P < 0.01). VO2 and AP decreased and were less after clonidine 4 micrograms kg-1 when compared with clonidine 2 micrograms kg-1 and placebo (P < 0.05) throughout the observation period. Thus, although clonidine 4 micrograms kg-1 attenuated the catecholamine response, the increases in VO2 and AP in response to CPT were similar in all groups.

The effect of clonidine or midazolam premedication on perioperative responses during ketamine anesthesia.

UNLABELLED: The use of ketamine as a sole anesthetic induces marked central sympathetic stimulation, causing increased heart rate, blood pressure (BP), and oxygen consumption (VO2). Both alpha 2-agonists and benzodiazepines have been used to attenuate these potentially harmful ketamine-induced responses. This double-blind, randomized, placebo-controlled study was designed to compare the perioperative metabolic, hemodynamic, and sympathoadrenal responses to IM clonidine (2 micrograms/kg) and midazolam (70 micrograms/kg) premedication during ketamine anesthesia. VO2 was measured continuously using indirect calorimetry in 30 ASA physical status I patients. The patients received ketamine, mivacurium, and fentanyl for the induction of anesthesia. Anesthesia was maintained using a ketamine infusion and fentanyl boluses i.v. Preoperatively, both VO2 and BP decreased significantly after the administration clonidine and midazolam compared with placebo (P < 0.01). Intraoperatively, VO2 was higher in the midazolam group than in the placebo and clonidine groups (P < 0.05). Postoperatively, there were no significant differences in BP and VO2, although they stayed at lower level in the clonidine group during the whole postoperative period. Clonidine decreased pre- and postoperative plasma catecholamine concentrations (P < 0.05). Our results indicate that a midazolam-ketamine combination may induce potentially harmful metabolic stimulation, whereas the sympatholytic effects of clonidine on ketamine-anesthetized patients may be beneficial, as perioperative VO2 was decreased. IMPLICATIONS: Ketamine causes sympathetic stimulation with an ensuing increase in oxygen consumption. Anticipating that clonidine might attenuate this response, we measured oxygen consumption in patients undergoing surgery during ketamine anesthesia. Patients treated with a clonidine-ketamine combination had lower intra- and postoperative oxygen consumption than those treated with a midazolam-ketamine combination.

Effect of clonidine and dexmedetomidine premedication on perioperative oxygen consumption and haemodynamic state.

Premedication has been shown to affect both oxygen consumption and metabolic rate. We have compared the perioperative metabolic and haemodynamic effects of two alpha 2-agonists, clonidine and the more selective dexmedetomidine, in 30 ASA I patients undergoing plastic surgical procedures under general anaesthesia. Patients were premedicated with clonidine 4 micrograms kg-1 (n = 10), dexmedetomidine 2.5 micrograms kg-1 (n = 10) or saline (n = 10) i.m. The doses of clonidine and dexmedetomidine were intended to be equipotent. The maximum decrease in preoperative oxygen consumption was 8% and decreases in systolic and diastolic arterial pressures were 11% from baseline after clonidine and dexmedetomidine. During operation, the maximum reduction in heart rate was 18% in the clonidine and dexmedetomidine groups compared with the placebo group. After operation, the maximum decrease in systolic arterial pressure was 11%, diastolic arterial pressure 15% and oxygen consumption 17% in the clonidine and dexmedetomidine groups compared with placebo. In summary, both clonidine 4 micrograms kg-1 and dexmedetomidine 2.5 micrograms kg-1 decreased perioperative oxygen consumption effectively, with a similar haemodynamic profile.