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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 E1on 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 E1was 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.

Severe pulmonary hypertension (PH) can be a critical problem during and after cardiac surgery, since it increases right ventricular afterload resulting in decreased cardiac output. A case of pulmonary hypertension associated with mitral valve disease and resistant to glyceryl trinitrate therapy during surgery is reported. The case was treated successfully with prostaglandin E1(PGE1), indicating that PGE1can be used peri-operatively in a patient with refractory PH resistant to glyceryl trinitrate treatment.