Pharmacologic neuroprotection in ischemic brain injury after cardiac arrest

• Published in: Annals of the New York Academy of Sciences Vol. 1507; no. 1; pp. 49 - 59
• Main Authors: Katz, Alyson, Brosnahan, Shari B., Papadopoulos, John, Parnia, Sam, Lam, Jason Q.
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.01.2022
• Subjects: Animals; Antibiotics; Antioxidants - administration & dosage; Ascorbic acid; Aspirin; Brain; Brain Injuries - etiology; Brain Injuries - metabolism; Brain Injuries - prevention & control; Brain injury; Brain Ischemia - etiology; Brain Ischemia - metabolism; Brain Ischemia - prevention & control; Cardiac arrest; Cell death; Cerebral blood flow; Coenzyme Q10; Defibrillators; Excitotoxicity; Head injuries; Heart; Heart Arrest - complications; Heart Arrest - drug therapy; Heart Arrest - metabolism; Humans; Hypoxia; inflammation; Ischemia; ischemia‐reperfusion; Magnesium; Memantine; Memantine - administration & dosage; Methylene blue; Minocycline; Mitochondria; mitochondrial dysfunction; Morbidity; Neuroprotection; Neuroprotection - drug effects; Neuroprotection - physiology; Neuroprotective Agents - administration & dosage; Nitriles - administration & dosage; Oxidative stress; Oxidative Stress - drug effects; Oxidative Stress - physiology; Pharmacology; Propofol; Pyridones - administration & dosage; Reperfusion; Steroid hormones; Thiamine; Thiamine - administration & dosage; Traumatic brain injury; Vitamin E; inflammation; neuroprotection; mitochondrial dysfunction; ischemia-reperfusion; excitotoxicity; cardiac arrest; oxidative stress
• ISSN: 0077-8923; 1749-6632; 1749-6632
• DOI: 10.1111/nyas.14613

Cardiac arrest has many implications for morbidity and mortality. Few interventions have been shown to improve return of spontaneous circulation (ROSC) and long‐term outcomes after cardiac arrest. Ischemic‐reperfusion injury upon achieving ROSC creates an imbalance between oxygen supply and demand. Multiple events occur in the postcardiac arrest period, including excitotoxicity, mitochondrial dysfunction, and oxidative stress and inflammation, all of which contribute to ongoing brain injury and cellular death. Given that complex pathophysiology underlies global brain hypoxic ischemia, neuroprotective strategies targeting multiple stages of the neuropathologic cascade should be considered as a means of mitigating secondary neuronal injury and improving neurologic outcomes and survival in cardiac arrest victims. In this review article, we discuss a number of different pharmacologic agents that may have a potential role in targeting these injurious pathways following cardiac arrest. Pharmacologic therapies most relevant for discussion currently include memantine, perampanel, magnesium, propofol, thiamine, methylene blue, vitamin C, vitamin E, coenzyme Q10, minocycline, steroids, and aspirin. Multiple events in the postcardiac arrest period contribute to ongoing brain injury. Given that complex pathophysiology underlies global brain hypoxic ischemia, neuroprotective strategies targeting multiple stages of the neuropathologic cascade should be considered as a means of mitigating secondary neuronal injury and improving neurologic outcomes and survival in cardiac arrest victims. In this review article, we discuss a number of different pharmacologic agents that may have a potential role in targeting these injurious pathways following cardiac arrest.