Hemodynamic characterization of cardiac dysfunction after traumatic brain injury using a controlled cortical impact model in male rats.

Traumatic brain injury (TBI) is associated with cardiovascular dysfunction that worsens clinical outcomes, yet the underlying mechanisms are poorly understood. Clinical studies are limited by heterogeneity, highlighting the need for controlled experimental models. Controlled cortical impact (CCI) provides precise control of injury severity, and invasive pressure-volume (PV) loop analysis allows detailed hemodynamic assessment. Adult male Wistar rats underwent sham operation or mild or severe CCI-induced TBI. PV-loop assessment and transthoracic echocardiography were performed at 8 or 24 h after TBI or sham. Serum epinephrine (EPI) and norepinephrine (NE) were quantified by ELISA. At 8 h post-injury, mild TBI was associated with decreased EES (p = 0.013) and increased V120 (p = 0.016), accompanied by qualitative global hypokinesis on echocardiography. Severe TBI demonstrated decreased cardiac output (p = 0.009) and stroke work (p = 0.006), whereas load-independent systolic indices were unchanged. At 24 h post-injury, severe TBI exhibited persistent global cardiac dysfunction. Serum NE and EPI were similar to shams; however, the NE-to-EPI ratio was decreased 8 h after mild TBI (p = 0.042). These findings suggest that TBI is associated with cardiovascular dysfunction that varies with injury severity; however, temporal characterization following mild TBI requires further study. Controlled experimental models provide a valuable platform for elucidating brain-heart interactions after TBI.