Traumatic-Brain Injury and Cardiovascular Diseases: Oxidative Stress at the Crossroad Linking TBI-Induced Autonomic Dysfunction to Cardiovascular Impairment

Traumatic brain injury (TBI) represents a major public health concern and presents a significant health care and economic burden to various countries and is one of the leading causes of death worldwide. One of the systemic alterations associated with TBI is cardiovascular impairments. This is primarily mediated through post-TBI cardiac autonomic dysfunction (CAD), which distorts the homeostasis of the autonomic nervous system. CAD post-TBI is usually preceded by several cellular and molecular alterations, among which are neural and systemic oxidative stress. Oxidative stress is implicated in the pathologies of cardiovascular disorders and also plays a significant role in aggravating post-TBI deficits. Cardiac cells contain NADPH oxidases (NOx) which, following TBI, cause increased production of reactive oxygen species (ROS), which reduces nitric oxide bioavailability to the endothelium, impairs endothelial vasodilation, and alters endothelial function. The resulting endothelial impairments predispose to cardiovascular dysfunction. In addition, TBI causes an increased release of catecholamines, which cause the alteration of the autonomic nervous system (ANS), specifically through sympathetic hyperactivity. Although CAD is a direct effect of TBI-induced alteration of the ANS, it disrupts cellular processes which result in increased production of ROS, thereby leading to more organ-wide dysfunction including cardiovascular impairment. This chapter highlights the link between TBI and cardiovascular impairments, and how ROS plays a significant role in TBI-induced cardiovascular dysfunction.