Effect of oxidative stress in rostral ventrolateral medulla on sympathetic hyperactivity after traumatic brain injury

• Published in: The European journal of neuroscience Vol. 50; no. 2; pp. 1972 - 1980
• Main Authors: Chen, Jigang, Chen, Wen, Han, Kaiwei, Qi, Enbo, Chen, Rongbin, Yu, Minkun, Hou, Lijun, Lv, Liquan
• Format: Journal Article
• Language: English
• Published: France Wiley Subscription Services, Inc 01.07.2019
• Subjects: Animal models; Blood pressure; Congestive heart failure; Hyperactivity; Malondialdehyde; Medulla oblongata; Microinjection; Norepinephrine; Oxidation; Oxidative stress; Reactive oxygen species; rostral ventrolateral medulla; Superoxide dismutase; sympathetic hyperactivity; Sympathetic nervous system; Tempol; Traumatic brain injury; traumatic brain injury; rostral ventrolateral medulla; oxidative stress; sympathetic hyperactivity
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1111/ejn.14374

Sympathetic hyperactivity occurs in a subgroup of patients after traumatic brain injury (TBI). The rostral ventrolateral medulla (RVLM) is a key region for the activity of sympathetic nervous system. Oxidative stress in the RVLM is proved to be responsible for the increased level of sympathetic activity in animal models of hypertension and heart failure. In this study, we investigated whether oxidative stress in the RVLM contributed to the development of sympathetic hyperactivity after TBI in rats. Model of diffuse axonal injury was induced using Sprague‐Dawley rats, and level of mean arterial pressure (MAP) and plasma Norepinephrine (NE) was measured to evaluate the sympathetic activity. For the assessment of oxidative stress, expression of reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) in the RVLM was determined. Microinjection of Tempol into the RVLM was performed to determine the effect of oxidative stress on sympathetic hyperactivity. According to the results, TBI led to elevated MAP and plasma NE in rats. It also induced a significantly increased level of ROS, MDA production and decreased level of SOD in the RVLM. The sympathetic activity, ROS, and MDA in the RVLM decreased significantly after microinjection of Tempol. Therefore, the present results suggested that oxidative stress in the RVLM was involved in the development of sympathetic hyperactivity following TBI. Microinjection of Tempol into the RVLM led to a decreased level of oxidative stress in the RVLM (A: ROS; B: MDA; C: SOD), and correspondingly the decreased level sympathetic activity (D: MAP; E: NE). It demonstrated that oxidative stress in the RVLM was involved in the development of sympathetic hyperactivity following TBI.