Effects of postconditioning with N,N,N'N'-tetrakis-2-pyridylmethyl-ethylenediamine in isolated rat hearts.
10.4097/kjae.2010.58.3.290
- Author:
Joon Hong KIM
1
;
Joon KIM
;
Yong Hyeon PARK
;
Kook Jin CHEUN
;
Young Ho JANG
Author Information
1. Department of Anesthesiology and Pain Medicine, Pureun Burn Hospital, Daegu, Korea. weonjo@pnuyh.co.kr
- Publication Type:Original Article
- Keywords:
Heart;
Myocardial stunning;
Postconditioning;
Reperfusion injury
- MeSH:
Animals;
Ethylenediamines;
Heart;
Ischemia;
Myocardial Infarction;
Myocardial Stunning;
Rats;
Reperfusion;
Reperfusion Injury
- From:Korean Journal of Anesthesiology
2010;58(3):290-295
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: It was reported that N,N,N'N'-tetrakis-[2-pyridylmethyl]-ethylenediamine (TPEN), a transition metal chelator, confers cardioprotection against myocardial ischemic injury. In this study, we investigated the effect of TPEN targeting reperfusion period in isolated rat hearts. METHODS: Langendorff perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Hearts were randomly assigned to either control (n = 9) or 10 micrometer of TPEN (n = 8) groups. TPEN was perfused for a period of 5 min before and 30 min after reperfusion. RESULTS: The ratio of infarct area/ischemic area (AN/AR) was significantly reduced in TPEN treated hearts (6.9 +/- 1.7%, P < 0.001) compared to control hearts (29.5 +/- 3.2%). Recovery of left ventricular developed pressure (LVDP), rate-pressure product (RPP), +dP/dt(max), and -dP/dt(min) in the control group after reperfusion were 53.8 +/- 6.2%, 51.0 +/- 6.3%, 51.9 +/- 5.7%, and 51.4 +/- 5.7%, respectively, of the baseline levels. In the TPEN group, LVDP, RPP, +dP/dt(max), and -dP/dt(min) returned to 58.5 +/- 4.6%, 54.8 +/- 6.4%, 61.7 +/- 4.9%, and 53.4 +/- 3.9%, respectively, of the baseline levels. There were no significant differences in the cardiodynamic variables between the two groups (P > 0.05). CONCLUSIONS: Pharmacological postconditioning with TPEN reduces myocardial infarction however, TPEN does not modify post-ischemic systolic dysfunction in isolated rat hearts.
