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Bucillamine prevents myocardial reperfusion Injury
Journal article   Open access   Peer reviewed

Bucillamine prevents myocardial reperfusion Injury

Lawrence D Horwitz and Nancy A Sherman
Journal of cardiovascular pharmacology, Vol.38(6), pp.859-867
12/2001
DOI: 10.1097/00005344-200112000-00007
PMID: 11707689
url
https://doi.org/10.1097/00005344-200112000-00007View
Published (Version of record) Open Access

Abstract

Injury during reperfusion can partially offset the benefit of relief of ischemia in myocardial infarctions rapidly treated with thrombolytic drugs or angioplasty. We assessed whether bucillamine (N-[2-mercapto-2-methylpropionyl]-L-cysteine) is potentially useful to treat myocardial reperfusion injury. Bucillamine is a potent sulfhydryl donor not previously tested as a treatment of reperfusion injury. Cardiac myocytes were exposed to hydrogen peroxide or a xanthine/xanthine oxidase system resulting in injury-induced release of lactate dehydrogenase. Bucillamine (125–500 μM) prevented lactate dehydrogenase release in a concentration-dependent manner. Bucillamine, which has two donatable thiol groups, was twice as protective as N-2-mercaptopropionyl glycine, which contains a single donatable thiol group. Dogs were then exposed to 90 min of coronary artery occlusion and 48 h of reperfusion before sacrifice. Beginning at the onset of reperfusion, bucillamine, 11 or 22 mg/kg per hour, or vehicle (saline) was administered intravenously for 3 h. There was a dose-related response to bucillamine for infarct size, normalized for size of the region at risk and adjusted for collateral blood flow to the ischemic region. Infarct size was reduced by 41% in the group treated with bucillamine 22 mg/kg per hour, compared with the vehicle group. Bucillamine, probably through an antioxidant mechanism, reduced infarct size when administered during reperfusion.
Cardiovascular System Antianginal agents. Coronary vasodilator agents Biological and medical sciences Medical sciences Pharmacology. Drug treatments

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