Abstract
This study evaluated the effect of mechanogated membrane ion channel blockers on brain catalase (CAT) activity and thiobarbituric acid reactive substances (TBARS) production after traumatic brain injury (TBI). A weight drop trauma model was used. Controls were sham-operated and received no weight drop. Gadolinium (GAD) or amiloride (AMI) were administered to control and experimental rats (30 min after TBI). Brain CAT activity and TBARS production were measured. When blood vessels were washed out with saline perfusion brain CAT activity significantly increased up to 6 h after trauma, decreasing significantly by 24 h; GAD or AMI administration preserved CAT activity 24 h after TBI. TBARS production increased after trauma, this effect being significantly reversed by GAD or AMI administration. GAD significantly decreased TBARS production in control animals. Mechanogated membrane ion channels may be involved in the genesis of the ionic disruption leading to oxidative stress and other secondary injury processes in head trauma.
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