Abstract

Introduction. Traumatic brain injury makes the brain vulnerable to secondary insults. Post-traumatic alterations in intracranial dynamics, such as reduced intracranial compliance (IC), are thought to further potentiate the effects of secondary insults. Reduced IC combined with intracranial volume insults leads to metabolic disturbances in a rat model. The aim of the present study was to discern whether a post-traumatic hypotensive insult in combination with reduced IC caused more pronounced secondary metabolic disturbances in the injured rat brain.Materials and methods. Rats were randomly assigned to four groups (n = 8/group): 1) trauma with hypotension; 2) trauma and reduced IC with hypotension; 3) sham injury with hypotension; and 4) sham injury and reduced IC with hypotension. A weight drop model of cortical contusion trauma was used. IC was reduced by gluing rubber film layers on the inside of bilateral bone flaps before replacement. Microdialysis probes were placed in the perimeter of the trauma zone. Hypotension was induced 2 h after trauma. Extracellular (EC) levels of lactate, pyruvate, hypoxanthine, and glycerol were analyzed.Results. The trauma resulted in a significant increase in EC dialysate levels of lactate, lactate/pyruvate ratio, hypoxanthine, and glycerol. A slight secondary increase in lactate was noted for all groups but group 2 during hypotension, otherwise no late effects were seen. There were no effects of reduced IC.Discussion. In conclusion, reduced IC did not increase the metabolic disturbances caused by the post-traumatic hypotensive insult. The results suggest that a mild to moderate hypotensive insult after initial post-traumatic resuscitation may be tolerated better than an early insult before resuscitation.

Highlights

  • Traumatic brain injury makes the brain vulnerable to secondary insults

  • The present study shows that a late hypotensive insult, following a focal traumatic brain injury, affects brain

  • The results from this study are similar to the metabolic and membrane responses seen after diffuse axonal injury combined with late hypotension and hypoxia [24]

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Summary

Introduction

Traumatic brain injury makes the brain vulnerable to secondary insults. Post-traumatic alterations in intracranial dynamics, such as reduced intracranial compliance (IC), are thought to further potentiate the effects of secondary insults. Despite promising results from experimental drug trials, none of the clinical trials of new drugs have been able to show a significant effect on outcome for TBI patients [2] It appears that further improvements in care require continued focus on pathophysiological mechanisms responsible for the enhanced vulnerability of the brain to secondary insults after trauma. Systemic hypotension is an insult that occurs in 15%–35% of patients with severe head injury and is associated with a significant increase in mortality and morbidity [9,10,11,12,13,14,15,16] A recent clinical study has shown that post-traumatic hypotension independently increased the risk of mortality, but it did not increase mortality in TBI patients more than it did for non-TBI patients [18]

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