Abstract
A study was carried out on 30 normotensive patients (American Society of Anesthesiologists physical status 1) to investigate whether or not a suppressive effect of 0.3 or 0.6 μg/kg prostaglandin E1 on the hypertensive response to tracheal intubation was due to inhibition of the increase in plasma catecholamine concentrations following the stressful stimulation. A total of 30 patients in three groups underwent elective surgery. Anaesthesia was induced with 5 mg/kg sodium thiopentone given intravenously and tracheal intubation was facilitated by 0.2 mg/kg vecuronium. Either saline (group A) or 0.3 (group B) or 0.6 μg/kg (group C) prostaglandin E1 was administered intravenously 15 s before direct laryngoscopy (lasting 30 s) which was attempted 2 min after administering thiopentone and vecuronium. All groups exhibited significant (P < 0.05) increases in mean arterial pressure, heart rate, rate – pressure product and plasma noradrenaline concentrations following tracheal intubation, but the increases in mean arterial blood pressure and rate – pressure product were significantly (P < 0.05) less in groups B and C than in group A. Prostaglandin E1, however, enhanced the increase in plasma noradrenaline concentrations following intubation. Data suggest that attenuation of the pressor response to intubation by prostaglandin E1, may not be due to inhibition of the noradrenaline release stimulated by intubation but to inhibition of noradrenaline-induced vasoconstriction.
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