Prostaglandin E1 and Tracheal Intubation: Relationship between the Cardiovascular Responses and Plasma Catecholamine Concentrations

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 E 1 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 E 1 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 E 1 , however, enhanced the increase in plasma noradrenaline concentrations following intubation. Data suggest that attenuation of the pressor response to intubation by prostaglandin E 1 , may not be due to inhibition of the noradrenaline release stimulated by intubation but to inhibition of noradrenaline-induced vasoconstriction.