British Journal of Anaesthesia, Vol 75, Issue 5 593-597, Copyright © 1995 by The Board of Management and Trustees of the British Journal of Anaesthesia
M. Tanaka and T. Nishikawa
It has been suggested that postjunctional alpha 1-adrenoceptor mediated
vasoconstriction is enhanced by clonidine. We have examined in humans if
the pressor responses to noradrenaline and phenylephrine are enhanced by
clonidine premedication. Seventy-seven patients were allocated randomly to
either clonidine (n = 38) or control (n = 39) groups. Patients in the
clonidine group received approximately 5 micrograms kg-1 with famotidine 20
mg, while the control group received famotidine 20 mg alone orally, 90 min
before induction of general anaesthesia with thiamylal. In all patients the
lungs were ventilated mechanically via tracheal tubes and anaesthesia
maintained with 1% end- tidal enflurane and 67% nitrous oxide in oxygen.
When a stable haemodynamic state was obtained, either noradrenaline 0.5
microgram kg- 1 (n = 40) or phenylephrine 2 micrograms kg-1 (n = 37) was
administered randomly i.v. as a bolus, while arterial pressure and heart
rate were measured noninvasively at 1-min intervals for 10 min. Although
noradrenaline caused significantly greater increases in mean arterial
pressure (MAP) in the clonidine group (from 2 to 4 min after i.v.
injection) compared with the control group, there were no significant
differences in the mean maximal increment in MAP or area under the MAP
curve between the two groups. However, i.v. phenylephrine produced a
significantly greater increase in MAP from 2 to 7 min (P < 0.05), and
greater mean maximal increase in MAP from the baseline value (21 (9) vs 14
(7) mm Hg; P < 0.05) in the clonidine than in the control group. In
addition, the duration of elevated MAP in the clonidine group was
significantly longer than that in the control group (7.6 (2.4) vs 5.1 (2.8)
min; P < 0.01). Furthermore, the area under the curve for MAP changes
after i.v. phenylephrine in the clonidine group was significantly greater
than that in the control group (69.7 (64.3) vs 11.5 (64.0) mm Hg min; P
< 0.01). There were no significant differences in arterial pressure or
heart rate after the pressor agents between the groups. There were no
significant differences between groups in the incidence of hypertension,
arrhythmia or bradycardia before or after i.v. noradrenaline or
phenylephrine. These results indicate that the pressor response to
phenylephrine, but not to noradrenaline, is augmented in patients with
clonidine premedication.
CLINICAL INVESTIGATIONS
Effects of clonidine premedication on the pressor response to alpha- adrenergic agonists
Department of Anaesthesia/Critical Care Medicine, Tsuchiura Kyodo General Hospital, 11-7 Manabeshinmachi, Tschiura-shi, Ibaraki-ken 300, Japan; Department of Anaesthesiology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan
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