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Shock-induced cytoplasmic NADH fluorescence changes in the living cat brain cortex: effect of dexamethasone
Insights
Dexamethasone pretreatment reduced NADH fluorescence and cortical vasodilatation during hemorrhagic shock in cats. However, it did not prevent decreased oxygen tension or electrocorticogram deterioration.
Area of Science:
- Neuroscience
- Pharmacology
- Physiology
Background:
- Hemorrhagic shock can lead to significant changes in cerebral cortex function.
- Understanding the effects of pharmacological interventions like dexamethasone is crucial for managing shock-related brain injury.
Purpose of the Study:
- To investigate the impact of dexamethasone on cerebrocortical physiology during hemorrhagic shock.
- To assess dexamethasone's ability to mitigate shock-induced alterations in NADH fluorescence, blood flow, oxygen tension, and electrocorticogram (ECoG).
Main Methods:
- Experiments were conducted on anesthetized cats subjected to induced hemorrhagic shock.
- Measurements included cerebrocortical NADH fluorescence, blood flow, blood volume, intracellular oxygen tension, and ECoG.
- Dexamethasone was administered prior to shock induction in treated groups.
Main Results:
- Dexamethasone did not alter baseline blood flow, volume, NADH fluorescence, or oxygen tension.
- Hemorrhagic shock caused increased cytoplasmic NADH fluorescence, an effect significantly blunted by dexamethasone.
- Dexamethasone pretreatment reduced shock-induced cortical vasodilatation but did not prevent decreased oxygen tension or ECoG deterioration.
Conclusions:
- Dexamethasone exhibits protective effects against certain metabolic and vascular changes in the cerebral cortex during hemorrhagic shock.
- Reduced cytoplasmic NAD reduction and potential lactate acidosis may contribute to dexamethasone's edema-controlling properties in pathological conditions.
Abstract:
The effect of dexamethasone administration on cerebrocortical NADH fluorescence, blood flow and blood volume, intracellular oxygen tension and electrocorticogram (ECoG) was studied in anaesthetized cats in two sets of experiments. Haemorrhagic shock was induced by stepwise decrease of mean arterial blood pressure from the control level a to 80, 60 and 40 mmHg. The bleeding was followed by reinfusion of the shed blood. The method of producing shock was identical in the untreated and dexamethasone treated groups. Dexamethasone was administered in the control period. The results are summarized as follows: (a) Dexamethasone, given in pharmacological doses failed to alter blood flow or blood volume, NADH fluorescence and the intracellular oxygen tension in the cerebral cortex of the cat; (b) Haemorrhagic shock resulted in a marked increase of cytoplasmic NADH fluorescence in the untreated group, while these changes were much smaller in the dexamethasone pretreated animals; (c) Dexamethasone pretreatment significantly reduced the extent of shock-induced cortical vasodilatation. In some experiments the brain cortex became ischaemic at 40 mmHg MABP; (d) Dexamethasone pretreatment failed to eliminate the shock-induced decrease in cortical intracellular oxygen tension and the irreversible deterioration of ECoG. It is suggested that the decrease in cortical cytoplasmic NAD reduction and the concomitant lactate acidosis might be involved in the ability of dexamethasone to control oedema during shock and other pathological conditions.