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Cardioprotective Effects of Acetaminophen Against H2O2 Injury
Author(s) -
Jaques Kathryn Michelle,
Golfetti Roseli,
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.a1374-b
Subject(s) - acetaminophen , medicine , anesthesia , ventricular tachycardia , peroxynitrite , bolus (digestion) , hydrogen peroxide , cardiology , pharmacology , superoxide , chemistry , biochemistry , enzyme
Acetaminophen has been shown to exhibit cardioprotective effects in the injured myocardium. During ischemia/reperfusion, reactive oxygen species such as superoxide, hydrogen peroxide, hydroxyl radical, and peroxynitrite are released. These radicals cause cellular damage, including release of potassium. Here we report our ongoing investigation of effects of acetaminophen on H 2 O 2 induced canine myocardial dysfunction. Left ventricular ±dP/dt max (mmHg/s), LVDP (mmHg), and RPP (mmHg/s) were measured in anesthetized open‐chest dogs after infusion of elevated H 2 O 2 . Left ventricular function varied significantly between vehicle and acetaminophen groups (see table below; ∗ P<0.05). Moreover, the incidence of H 2 O 2 induced ventricular arrhythmias varied between vehicle and acetaminophen groups. Percent ectopy following high dose H 2 O 2 , was 1.2±.4 vs. 0.3±.1 (p<0.05) for vehicle and acetaminophen treated dogs respectively. In one case, at baseline settings, spontaneous ventricular tachycardia occurred and was attenuated by 15 mg/kg acetaminophen bolus. We conclude that acetaminophen is both cardioprotective and antiarrhythmic against administered H 2 O 2 in the canine myocardium. This work was funded in part by Johnson & Johnson COSAT/McNeil CSP.