Effect of aminoguanidine on ischemia-reperfusion induced myocardial injury in rats

Parlakpinar H., Ozer M., Acet A.

MOLECULAR AND CELLULAR BIOCHEMISTRY, vol.277, pp.137-142, 2005 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 277
  • Publication Date: 2005
  • Doi Number: 10.1007/s11010-005-5779-9
  • Journal Indexes: Science Citation Index Expanded, Scopus
  • Page Numbers: pp.137-142


Myocardial ischemia-reperfusion (MI/R) has been implicated in the induction of inducible nitric oxide synthase (iNOS) that leads to increase production of nitric oxide (NO). Recently, excessive production of NO has been involved in causing myocardial injury. In our in vivo model, we examined the effects of aminoguanidine (AMG), a known iNOS inhibitor, on percentage infarct size in anaesthetized rats. A total of 14 rats were equally divided into two groups (n = 7 in each group). To produce myocardial necrosis, the left main coronary artery was occluded for 30 min, followed by 120 min of reperfusion, in anesthetized rats. AMG (200 mg kg(-1)) was given intravenously 10 min before occlusion. The volume of infarct size and the risk zone were determined by planimentry of each tracing and multiplying by the slice thickness. Infarct size was normalized by expressing it as a percentage of the area at risk. Hemodynamic parameters were measured via the left carotid artery. Compared to MI/R group, whereas AMG administration elevated mean arterial blood pressure, statistically reduced the myocardial infarct size (21 +/- 1 and 14 +/- 4%, respectively) and infract size/risk zone (53 +/- 3 and 37 +/- 5%, respectively) in rat model of ischemia-reperfusion. In conclusion, this study indicates that iNOS inhibitor, AMG, show reduction in NO's side effect in I/R injury.