Methylprednisolone (MP) at cardiac surgery has been shown to reduce perioperative proinflammatory cytokine responses, reduce neutrophil adhesion molecule expression and increase antiinflammatory interleukin-10 [1]. This effect has been linked with renal protection [2]. Paradoxically, MP administration has been associated with impaired pulmonary function [3]. The mechanism is unknown. To begin elucidating this, we investigated the hypothesis that methylprednisolone would significantly exacerbate porcine pulmonary dysfunction induced by infrarenal aortic ischaemia-reperfusion.

Forty-two male, 10–12 week old, pigs underwent pentobarbitone anaesthesia followed by tracheostomy and mechanical ventilation. The inspired oxygen concentration was maintained at 70% throughout the procedure and all animals had invasive monitoring of their systemic and pulmonary pressures. At laparotomy the infrarenal aorta was cross clamped for 150 min and then released to allow 180 min of reperfusion. The animals were randomly allocated to treatment (n = 21) or control groups (n = 21). After a baseline arterial blood sample was taken the treatment group received 30 mg/kg of MP and the control group a saline placebo. Arterial blood samples were obtained after 30, 60, 90, 120 and 150 min of ischaemia. Further samples were collected at 30, 60, 90, 120, 150 and 180 min into reperfusion.

During the ischaemia-reperfusion period all animals showed a time dependent deterioration in arterial oxygen tension (P < 0.05; Wilcoxon signed rank test). The PaO₂ was lower (P < 0.05) in the treatment group compared to the control group (Mann Whitney U test) during ischaemia at time points 60, 90 and 120 min and during the reperfusion period at 60, 90, 120, 150 and 180 min (Fig. 1).

This porcine model demonstrates MP induced exacerbation of ischaemia reperfusion related pulmonary dysfunction. This model will allow elucidation of the relative protective or deleterious effects of MP administration as well as mechanisms of action.