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Title page for ETD etd-12032017-114455

Type of Document Master's Thesis
Author Salzman, Michele Marie
URN etd-12032017-114455
Title Poloxamer 188 Protects Isolated Mouse Cardiomyocytes from Hypoxia/Reoxygenation Injury - Implications for Cardioprotection after Cardiac Arrest
Degree Master of Science
Department Pharmacology
Advisory Committee
Advisor Name Title
Joey V. Barnett, PhD Committee Chair
Janis T. Eells, PhD Committee Member
Jerod S. Denton, PhD Committee Member
Matthias L. Riess, MD, PhD Committee Member
  • polyethylene glycol (PEG)
  • FM1-43
  • Fluo-4
Date of Defense 2017-10-31
Availability restricted
Cardiac arrest is a leading cause of death. Even with the best cardiopulmonary resuscitation (CPR), many patients still die or suffer severe organ damage. The reintroduction of blood flow at the start of CPR after systemic ischemia causes additional damage to organs, such as the heart, beyond that caused by the ischemia itself. Ischemia/reperfusion (I/R) injury is a complex pathological event involving processes that can lead to disruptions in the cell membrane and cellular dysfunction. Loss of membrane integrity may allow an influx of calcium (Ca2+) into cardiomyocytes, leading to hypercontracture and cell death. Methods to improve the endogenous membrane resealing capacity of cells that are overwhelmed due to pathological disruptions, such as I/R injury, are needed to prevent cardiomyocyte death, because the ability of the myocardium to regenerate is limited. Using an in-vitro cardiomyocyte model exposed to simulated I/R (hypoxia/reoxygenation, H/R), the tri-block copolymer Poloxamer 188 (P188), with its unique hydrophobic/hydrophilic chemical properties, was administered during reoxygenation and assessed for its ability to provide membrane repair and cellular protection. P188 protected cardiomyocytes from H/R injury by repairing cell membranes, reducing LDH release, and decreasing Ca2+ influx. Additionally, it was shown that the majority of Ca2+ influx during H/R was through tears in the cell membrane, which were targeted by P188, rather than through Ca2+ channels and exchangers not targeted by P188. Determining the mechanism of action of a compound administered during CPR on the cellular dysfunction caused during I/R injury could aid to improve CPR practices in the future.
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