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Potential cerebroprotective effects of acetaminophen
Author(s) -
Baliga Sunanda,
Merrill Gary
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1221
Subject(s) - acetaminophen , stroke (engine) , medicine , pharmacology , anesthesia , mitochondrion , ischemia , reperfusion injury , chemistry , biochemistry , mechanical engineering , engineering
Incidence of stroke in the United States has been steadily increasing, making it the third leading cause of death. There is a paucity of treatments for stroke and they are expensive to obtain. Therefore, use of a readily available, inexpensive drug to minimize the damage of stroke would be welcome. Acetaminophen has antioxidant properties that can combat tissue damage caused by ischemia/reperfusion. We have published data demonstrating the efficacy of acetaminophen in the injured mammalian myocardium. In that setting, acetaminophen significantly decreases the concentration of hydroxyl radicals and peroxynitrite while preserving myofibrillar ultrastructure. Other labs have shown similar oxidants produced upon reperfusion in stroke. These observations prompted us to investigate the potential cerebroprotective role of acetaminophen during stroke. Male Sprague Dawley rats (350–400g) were divided into two groups: vehicle and acetaminophen treated. Rats underwent bilateral carotid artery occlusion (BCAO) combined with systemic hypotension (P ~40–50 mmHg) for 15 minutes followed by 45 minutes of reperfusion. Acetaminophen (15 mg/kg i.v.) was administered after ex‐sanguination. Brains were fixed and extracted for electron microscopy (EM). Vehicle treated rat brains appeared to sustain greater mitochondrial damage than corresponding acetaminophen treated brains. (Fig. 1) This work was funded in part by Johnson & Johnson COSAT/McNeil CSP. 1Electronmicrographs of vehicle and acetaminophen rat brain. Arrows indicate ruptured mitochondria (A) and intact mitochondria (B).