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- Open Access
0036. Confocal imaging of impaired mitochondrial function in the cerebral cortex of rats during haemorrhagic shock in vivo
© Ida et al; licensee Springer. 2014
- Published: 26 September 2014
- Cerebral Cortex
- Mean Arterial Pressure
- Mitochondrial Function
- Mitochondrial Membrane Potential
- Cerebral Perfusion Pressure
Haemorrhagic shock (HS)-induced hypotension impairs cerebral perfusion pressure and decreases oxygen supply to the brain (1), but the consequences for brain mitochondrial function are poorly understood.
To investigate the effects of HS on mitochondrial function in the cerebral cortex of rats in vivo.
A flap of skull was removed and cerebral cortex exposed in isoflurane-anaesthetised rats undergoing HS (target mean arterial pressure (MAP) of 40 mmHg for 30 minutes) (n=7) compared with sham (n=6) controls. Mitochondrial function was assessed by observing mitochondrial membrane potential (using tetramethyl rhodamine methyl ester (TMRM); ex: 543 nm; em: 585 nm), and endogenous flavin adenine dinucleotide (FAD) autofluorescence (ex: 488 nm; em: 505-570 nm) by confocal imaging. The TMRM and FAD signals were registered before induction of HS (baseline), at MAP of 40 mmHg (shock), and at 30 (T30) and 60 (T60) minutes after shock.
HS-induced hypotension causes a marked loss of mitochondrial membrane potential and FAD fluorescence in cerebral cortex, except in regions in immediate proximity to arterioles. This study reveals a profound spatial vulnerability of cortical tissue to reduced blood flow.
Programa Ciência sem Fronteiras 10464-4-12, UK MS Society, MRC.
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