Yezan Abderrahman, MD
Pediatric Critical Care Fellow
University of Iowa Hospital and Clinics
Iowa City, IA, United States
Disclosure information not submitted.
Zili Luo, MD, PhD
Research Specialist, Pediatrics
University of Iowa Hospitals and Clinics
Iowa City, Iowa, United States
Disclosure information not submitted.
Noah Gilkes, n/a
Undergraduate student /Research Assistant, Pediatrics
University of Iowa Hospitals and Clinics
Iowa City, Iowa, United States
Disclosure information not submitted.
Shaunik Sharma, PhD
Postdoctoral Researcher, Pediatrics
University of Iowa Hospitals and Clinics
Iowa City, Iowa, United States
Disclosure information not submitted.
Robert Weiss, MD
Professor, Cardiology
University of Iowa Hospitals and Clinics, United States
Disclosure information not submitted.
Alexander Bassuk, MD, PhD
Professor, Pediatric Neurology
University of Iowa Hospitals and Clinics, United States
Disclosure information not submitted.
Elizabeth Newell, MD
Assistant Professor, Pediatric Critical Care
University of Iowa Hospitals and Clinics
Iowa City, Iowa, United States
Disclosure information not submitted.
Title: Cardiac Dysfunction and Immune Response Following Traumatic Brain Injury
Introduction: Following traumatic brain injury (TBI), central and peripheral immune responses have been implicated in contributing to secondary brain injury and prior work also indicates inflammation may contribute to effects on other organs. Recent literature also shows a role for the inflammatory response in mediating cardiac dysfunction in one animal based TBI model. Overall, only a paucity of data describes cardiac involvement in such setting. We hypothesized the presence of cardiac dysfunction following TBI and a potential role of inflammatory response in mediating such injury in the fluid percussion injury TBI model.
Methods: Adult, male C57BL/6J mice underwent craniectomy and were subjected to lateral fluid percussion injury or sham procedure. Echocardiography (echo) was done at baseline and at day 3 post-TBI (n=11) or sham (n=8). Blood pressure (BP) was also monitored and recorded simultaneously. Mice were euthanized at day 3 post-procedure. Heart tissues were isolated, perfused with 4% PFA, and coronally sectioned for immunohistochemistry (IHC). Antibodies against monocyte chemotactic protein-1 (MCP-1) and nicotinamide adenine dinucleotide phosphate oxidase-2 (NOX2) were employed. Another set of tissues was collected from left ventricle (LV) for RNA extraction, looking at acute proinflammatory cytokine expression of IL-1a, IL-1b, and TNF- α via RT-PCR (n=4/group). P-value ≤ 0.05 was considered as statistically significant.
Results: Increased signal was observed in some tissues for NOX2 and to a lesser extent MCP1 with no significant difference amongst groups. Additionally, no difference was observed between groups compared for BP and echo measurements of LV thickness, ejection fraction, cardiac output, end diastolic and systolic volumes. PCR analysis of cytokines IL-1a, IL-1b and TNF-α in LV region showed slight increase in IL-1a and TNF-α expression in TBI group but with no statistical significance.
Conclusions: Our model of TBI does not result in acute cardiac dysfunction. Hemodynamic variables and echocardiography measurements showed no statistical difference between TBI and sham groups. Furthermore, it appears that inflammatory response in the heart tissue following TBI in our model wasn’t remarkable compared to the sham group based on IHC studies and PCR analysis.