Original Contribution

Basic Research in Cardiology

, Volume 105, Issue 4, pp 513-522

Impact of acute myocardial ischemia reperfusion on the tissue and blood-borne renin–angiotensin system

  • Shizu OyamadaAffiliated withCardiovascular Research Center, Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University
  • , Cesario BianchiAffiliated withCardiovascular Research Center, Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University
  • , Shinji TakaiAffiliated withDepartment of Pharmacology, Osaka Medical College
  • , Michael P. RobichAffiliated withCardiovascular Research Center, Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University
  • , Richard T. ClementsAffiliated withCardiovascular Research Center, Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University
  • , Louis ChuAffiliated withCardiovascular Research Center, Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University
  • , Frank W. SellkeAffiliated withCardiovascular Research Center, Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University Email author 

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Abstract

We examined the impact of acute myocardial ischemia followed by reperfusion (AMI-R) on local and circulating renin–angiotensin system (RAS) in a swine model. The mid left anterior descending artery (n = 6) was occluded for 1 h, followed by reperfusion for 2 h. Monastryl blue/triphenyl tetrazolium chloride staining identified the area-at-risk (AAR) and infarction. A second group of control animals underwent sham operations (C: n = 4). Myocardial expression of angiotensinogen (AGT), renin, chymase, angiotensin converting enzyme (ACE), angiotensin II (Ang II), Ang II type1 receptor (AT1R) and Ang II type 2 receptor (AT2R) in the AAR and the non-ischemic left ventricle (NLV) was assessed. Serum level of these proteins at baseline and at the end of reperfusion was also examined. Chymase (P < 0.05), ACE (P < 0.05), Ang II (P < 0.05), AT1R (P < 0.05) and AT2R (P < 0.05) expressions were found to be significantly higher in the AAR compared to the NLV and C whereas no significant differences were found for AGT (P = 0.58) and renin (P = 0.38). Serum concentration of ACE was significantly higher at the end of reperfusion than at baseline (P < 0.01), whereas no significant difference was found for chymase (P = 0.71), AGT (P = 0.57) and Ang II (P = 0.19). Immunohistochemistry of myocardial sections demonstrated significantly higher expression of ACE (P = 0.02), AT1R (P = 0.01), AT2R (P = 0.02) and Ang II (P < 0.01) in the AAR as compared to the NLV, whereas no significant difference was found for renin (P = 0.39). In conclusion, AMI-R resulted in significantly higher expression of specific cardiac RAS components in AAR compared to the NLV in the acute period.

Keywords

Renin–angiotensin system Acute myocardial ischemia followed by reperfusion Left ventricular remodeling Angiotensin II Angiotensin II receptor