Explosive munitions account for more than 50% of all
wounds sustained in military combat, and the proportion of civilian casualties due to
explosives is increasing as well. But there has been only limited research on the pathophysiology of blast-induced
brain injury, and the contributions of alterations in cerebral blood flow (CBF) or cerebral vascular reactivity to blast-induced
brain injury have not been investigated. Although secondary
hypotension and
hypoxemia are associated with increased mortality and morbidity after
closed head injury, the effects of secondary insults on outcome after
blast injury are unknown.
Hemorrhage accounted for approximately 50% of combat deaths, and the lungs are one of the primary organs damaged by blast overpressure. Thus, it is likely that blast-induced
lung injury and/or
hemorrhage leads to hypotensive and hypoxemic secondary injury in a significant number of combatants exposed to blast overpressure injury. Although the effects of
blast injury on CBF and cerebral vascular reactivity are unknown,
blast injury may be associated with impaired cerebral vascular function.
Reactive oxygen species (ROS) such as the
superoxide anion radical and other ROS, likely major contributors to traumatic cerebral
vascular injury, are produced by
traumatic brain injury (TBI).
Superoxide radicals combine with
nitric oxide (NO), another ROS produced by
blast injury as well as other types of TBI, to form
peroxynitrite, a powerful
oxidant that impairs cerebral vascular responses to reduced intravascular pressure and other cerebral vascular responses. While current research suggests that
blast injury impairs cerebral vascular compensatory responses, thereby leaving the brain vulnerable to secondary insults, the effects of
blast injury on the cerebral vascular reactivity have not been investigated. It is clear that further research is necessary to address these critical concerns.