Effects of des-aspartate-angiotensin I on myocardial ischemia-reperfusion injury in rats

Qiang Wen, Meng Kwoon Sim*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


The present study investigated the actions of des-aspartate-angiotensin I (DAA-I) on infarct size and three early inflammatory events in acute myocardial ischemia-reperfusion injury in rats. The rationale was based on earlier findings showing that chronic daily administration of DAA-I attenuated infarct size of ischemic-reperfused rat heart, and cardiac hypertrophy in pressure overload rats. Anesthetized rats were subjected to 45 min of ischemia and 5 h of reperfusion. Infarcted area, serum creatine kinase, and tissue myeloperoxidase activity were determined. The expression of intercellular adhesion molecule-1 (ICAM-1) was also investigated by immunohistochemistry and Western blotting. Intravenous administration of DAA-I at 5 min post reperfusion reduced myocardial infarct size by 45.5%, lowered serum creatine kinase activity, decreased myeloperoxidase activity in cardiac tissue, and inhibited the expression of ICAM-1 in cardiac capillary endothelium. The maximum effective dose was 1013 pmol/kg, and the cardioprotective actions of DAA-I were blocked by indomethacin. The data showed that the cardioprotection accorded by DAA-I was the result of its anti-inflammatory actions on early inflammatory processes in myocardial ischemia-reperfusion injury. The anti-inflammatory processes were indomethacin sensitive and probably mediated by prostaglandins.

Original languageEnglish (US)
Pages (from-to)193-199
Number of pages7
JournalEuropean Journal of Pharmacology
Issue number2-3
StatePublished - May 11 2011


  • (Rat heart)
  • Des-aspartate-angiotensin I
  • Inflammation
  • Ischemia-reperfusion injury
  • Prostaglandin

ASJC Scopus subject areas

  • Pharmacology


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