Differences in cerebral reperfusion and oxidative injury after cardiac arrest in pigs
Article first published online: 11 AUG 2003
Acta Anaesthesiologica Scandinavica
Volume 47, Issue 8, pages 958–967, September 2003
How to Cite
Liu, X. L., Wiklund, L., Nozari, A., Rubertsson, S. and Basu, S. (2003), Differences in cerebral reperfusion and oxidative injury after cardiac arrest in pigs. Acta Anaesthesiologica Scandinavica, 47: 958–967. doi: 10.1034/j.1399-6576.2003.00189.x
- Issue published online: 11 AUG 2003
- Article first published online: 11 AUG 2003
- Accepted for publication 8 April 2003
- reperfusion injury;
- oxidative damage;
- free radical;
- cerebral haemodynamics;
Background: An investigation of the free radical scavenger sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) and the weak vasodilatator Tris buffer mixture (TBM) on cerebral cortical blood flow (CCBF) and the jugular bulb concentration of two eicosanoids, indicators of oxidative stress and inflammation, was undertaken in 30 anaesthetized piglets during cardiopulmonary resuscitation (CPR) and after restoration of spontaneous circulation (ROSC).
Methods: Thirty animals were subjected to 8 min of untreated circulatory arrest followed by 8 min of closed-chest CPR. During CPR, the animals were randomized to receive 60 mg/kg S-PBN, 1 mmol/kg TBM or 2 ml/kg normal saline (n = 10 in each group). Systemic haemodynamic variables, CCBF and jugular bulb plasma concentrations of 8-iso-PGF2α and 15-keto-dihydro-PGF2α were measured.
Results: The CCBF during reperfusion after ROSC was greater in the TBM group than in the S-PBN group, the regression coefficient between CCBF and mean arterial blood pressure being lower in the S-PBN group than in the TBM group. The jugular bulb plasma concentration of 8-iso-PGF2α during the first 30 min after ROSC was greater in the TBM group than in the S-PBN group. Administration of TBM after vasopressin did not attenuate the pressor effect of vasopressin.
Conclusion: Administration of S-PBN during CPR results in less cerebral oxidative stress, possibly by promoting normal distribution of cerebral blood flow.