Paul Silaghi
Pronouns: he/him
Research Mentor(s): Daniel Eitzman
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine – Cardiology / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 6 – 4:40pm – 5:30 pm
Room: League Ballroom
Authors: Paul Silaghi, Daniel Eitzman, Jessica Venugopal
Presenter: 3
Abstract
Beta-Adrenergic Blockade Prevents Accelerated Atherosclerosis Following Traumatic Brain Injury in Mice Background Traumatic Brain Injury (TBI) is associated with cardiovascular morbidity and mortality in humans. Recent studies in the Eitzman Lab demonstrated a causal relationship between TBI and accelerated atherosclerosis in a mouse model, along with sympathetic nervous system activation. The purpose of this study was to determine the effect of a beta-adrenergic receptor blocker, metoprolol, on atherosclerosis following TBI in mice. Methods This study was conducted on atherosclerotic-prone mouse models, which were fed a Western diet for 4 weeks before being subjected to a piston-induced traumatic brain injury or sham surgery. Following this, mice were randomized to metoprolol in drinking water (2mg/mL) or vehicle control. Mice were continued on a Western diet and were sacrificed after 6 weeks. Five-micron sections from the aortic root of their hearts were imaged using an upright microscope and analyzed with the Metamorph software. This software analysis used threshold color recognition to identify macrophages (through anti-mac3 antibodies) and calcium, with the greater presence of either one or both pointing to increased atherosclerosis. Results The results of this study found that the quantified amounts of macrophages and calcium, both contributors to atherosclerotic plaque size, were greater in mice with a TBI but were reduced with the administration of metoprolol. The amount of plaque calcium quantified was reduced in mice without a TBI after consuming metoprolol, while the quantification of macrophages remained almost unchanged. Furthermore, atherosclerotic lesion thickness (intima/media ratio) increased in TBI mice with vehicle treatment as compared to sham mice but was reduced in TBI mice that consumed metoprolol. Conclusion These results support the proposition that a traumatic brain injury has a causal relationship with an increase in the size of atherosclerotic plaques. This study also supports the potential of metoprolol, a common and widely-available drug, to treat and reduce TBI-induced atherosclerosis.
Biomedical Sciences
