Skip to main content

Methylprednisolone exacerbates porcine pulmonary dysfunction induced by infrarenal aortic ischaemia-reperfusion

Background

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.

Methods

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.

Results

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).

Figure 1
figure1

P < 0.05 (Mann–Whitney U test) for between group differences. Error bars display interquartile ranges. MP, methylprednisolone.

Conclusions

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.

References

  1. 1.

    Hill GE, Alonso A, Thiele GM, Robbins RA: Glucocorticoids blunt neutrophil CD11b surface glycoprotein upregulation during cardiopulmonary bypass in humans. Anesth Analg 1994, 79: 23-27.

    CAS  Article  PubMed  Google Scholar 

  2. 2.

    Baker RC, Armstrong MA, Barros D'Sa AAB, Campbell FC, McClean E, McBride WT: The effect of methylprednisolone on urinary N-acetyl-β-D-glucosaminidase/creatinine ratios in porcine vascular surgery. Br J Anaesth 2001, 87: 661P.

    Google Scholar 

  3. 3.

    Chaney MA, Nikolov MP, Blakeman B, Bakhos M, Slogoff S: Pulmonary effects of methylprednisolone in patients undergoing coronary artery bypass grafting and early tracheal extubation. Anesth Analg 1998, 87: 27-33. 10.1097/00000539-199807000-00007

    CAS  PubMed  Google Scholar 

Download references

Acknowledgements

This research is supported by the British Heart Foundation.

Author information

Affiliations

Authors

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Baker, R., Armstrong, M., Allen, S. et al. Methylprednisolone exacerbates porcine pulmonary dysfunction induced by infrarenal aortic ischaemia-reperfusion. Crit Care 5, 4 (2001). https://doi.org/10.1186/cc1436

Download citation

Keywords

  • Methylprednisolone
  • Ischaemia Reperfusion
  • Arterial Blood Sample
  • Pentobarbitone
  • Adhesion Molecule Expression