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Updated: Jul 20, 2026
A Swine Model of Neonatal Asphyxia
Published on: October 11, 2011
Reventilation with room air or 100% oxygen after asphyxia differentially affects cerebral neuropathology in newborn
Ferenc Domoki1, Aliz Zimmermann, Gabor Cserni
1Department of Physiology, Faculty of Medicine, University of Szeged, Szeged, and Department of Pathology, University Teaching Hospital, Kecskemét, Hungary. domoki@phys.szote.u-szeged.hu
Aim:
To test if reventilation with room air (RA) or 100% oxygen (O2) after asphyxia would differentially affect neuronal damage in different brain areas of newborn pigs.
Methods:
Anaesthetized piglets were subjected to 10 min asphyxia (n=27) or served as time controls (n=7). Reventilation started with either RA or O2 for 1 h, and was continued with RA for an additional 1-3 h. Cortical or cerebellar blood flow was assessed with laser-Doppler flowmetry (LDF). Haematoxylin/eosin-stained sections from six brain regions were prepared for blinded neuropathological examination and scoring.
Results:
Asphyxia resulted in significant neuronal damage compared to time controls in all areas examined except the pons. O2 ventilation elicited greater neuronal lesions in the hippocampus and the cerebellum but smaller damage in the basal ganglia compared to RA. The assessed physiological parameters including the LDF signals were similar in both ventilation groups, except for PaO2 in the first hour of reventilation (RA 75+/-5 mmHg, O2 348+/-57 mmHg; p<0.05). Interestingly, however, reactive hyperaemia was much higher in the O2-sensitive cerebellum as compared with the cortex (1101+/-227 vs 571+/-73; p<0.05, area under the curve).
Conclusion:
O2 toxicity after asphyxia was demonstrated in the piglet hippocampus and cerebellum but not in the cerebral cortex or basal ganglia. The observed regional differences may be associated with local haemodynamic factors.
