Dynamic FDG PET for assessing early effects of cerebral hypoxia and resuscitation in new-born pigs

  • Charlotte de Lange
  • Eirik Malinen
  • Hong Qu
  • Kjersti Johnsrud
  • Arne Skretting
  • Ola Didrik Saugstad
  • Berit H. Munkeby
Original Article

Abstract

Purpose

Changes in cerebral glucose metabolism may be an early prognostic indicator of perinatal hypoxic–ischaemic injury. In this study dynamic 18F-FDG PET was used to evaluate cerebral glucose metabolism in piglets after global perinatal hypoxia and the impact of the resuscitation strategy using room air or hyperoxia.

Methods

New-born piglets (n = 16) underwent 60 min of global hypoxia followed by 30 min of resuscitation with a fraction of inspired oxygen (FiO2) of 0.21 or 1.0. Dynamic FDG PET, using a microPET system, was performed at baseline and repeated at the end of resuscitation under stabilized haemodynamic conditions. MRI at 3 T was performed for anatomic correlation. Global and regional cerebral metabolic rates of glucose (CMRgl) were assessed by Patlak analysis for the two time-points and resuscitation groups.

Results

Global hypoxia was found to cause an immediate decrease in cerebral glucose metabolism from a baseline level (mean ± SD) of 21.2 ± 7.9 to 12.6 ± 4.7 μmol/min/100 g (p <0.01). The basal ganglia, cerebellum and cortex showed the greatest decrease in CMRgl but no significant differences in global or regional CMRgl between the resuscitation groups were found.

Conclusion

Dynamic FDG PET detected decreased cerebral glucose metabolism early after perinatal hypoxia in piglets. The decrease in CMRgl may indicate early changes of mild cerebral hypoxia–ischaemia. No significant effect of hyperoxic resuscitation on the degree of hypometabolism was found in this early phase after hypoxia. Cerebral FDG PET can provide new insights into mechanisms of perinatal hypoxic–ischaemic injury where early detection plays an important role in instituting therapy.

Keywords

Glucose metabolism FDG PET Perinatal hypoxia–ischaemia Piglet 

Notes

Acknowledgments

The authors thank the Child Foundation at Oslo University Hospital for their grant in support of this research. We are also grateful to the bioengineers of the Department of Nuclear Medicine for their help in performing the study.

Financial support

A grant from the Child Foundation at Oslo University Hospital.

Conflicts of interest

None.

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Copyright information

© Springer-Verlag 2012

Authors and Affiliations

  • Charlotte de Lange
    • 1
    • 3
  • Eirik Malinen
    • 2
    • 6
  • Hong Qu
    • 5
  • Kjersti Johnsrud
    • 3
  • Arne Skretting
    • 4
  • Ola Didrik Saugstad
    • 1
    • 7
  • Berit H. Munkeby
    • 1
  1. 1.Department of Paediatric ResearchOslo University Hospital, RikshospitaletOsloNorway
  2. 2.Department of Medical PhysicsOslo University HospitalOsloNorway
  3. 3.Department of Radiology and Nuclear MedicineOslo University Hospital, RikshospitaletOsloNorway
  4. 4.The Intervention CentreOslo University HospitalOsloNorway
  5. 5.Centre for Molecular Biology and Neuroscience, Department of Anatomy, Institute of Basic Medical SciencesUniversity of OsloOsloNorway
  6. 6.Department of PhysicsUniversity of OsloOsloNorway
  7. 7.Department of MedicineUniversity of OsloOsloNorway

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