z-logo
Premium
Brain death increases COX ‐1 and COX ‐2 expression in the renal medulla in a pig model
Author(s) -
HVAS C. L.,
NØRREGAARD R.,
NIELSEN T. K.,
BARKLIN A.,
TØNNESEN E.
Publication year - 2014
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/aas.12235
Subject(s) - medicine , medulla , renal medulla , kidney , pathology
Background Brain death is linked to a systemic inflammatory response that includes prostaglandins and cytokines among its mediators. The levels of cyclooxygenase‐1 and cyclooxygenase‐2 ( COX ‐1 and COX ‐2) affect graft survival, but it remains unknown whether these enzymes are modified during brain death. The aims of this study were to investigate the organ expression of COX and to analyse the cytokine response in the plasma, cerebrospinal fluid ( CSF ), and organs in a porcine model of intracerebral haemorrhage and brain death. Methods Twenty pigs were randomly assigned to either a brain death group or a control group. Brain death was induced by an intracerebral injection of blood, and the animals were observed over the next 8 h. Tissue samples were tested for COX ‐1, COX ‐2 messenger RNA ( mRNA ) expression (heart, lung, and kidney), haeme oxygenase‐1 ( HO ‐1) (kidney), interleukin‐1 β ( IL ‐1 β ), IL ‐6, IL ‐8, IL ‐10, and tumour necrosis factor‐α. These cytokines were also measured at eight time points in the plasma and CSF . Results At the organ level, the levels of COX ‐1 and COX ‐2 mRNA expression were increased only in the renal medulla ( P  = 0.03 and P  = 0.02, respectively). The cytokine levels in the tissue, plasma, and CSF revealed no differences between the groups. HO ‐1 expression decreased ( P  = 0.0088). Conclusion Brain death increases the expression of COX ‐1 and COX ‐2 mRNA in the renal medulla. The release of cytokines into the plasma and CSF did not vary between the groups.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here