Research article summary (published 30 Jul 2004):

Stunned peri-infarct canine myocardium is characterized by degradation of troponin T, not troponin I.

Full Abstract

OBJECTIVE: Degradation of cardiac troponin I (cTnI) has been proposed to represent the underlying molecular mechanism responsible for post-ischemic contractile dysfunction of viable but 'stunned' myocardium. However, this concept is largely derived from models of brief, sublethal ischemia essentially devoid of necrosis, and there is speculation that defects in cTnI may be model-dependent. Accordingly, our primary aim was to evaluate the integrity of cardiac troponins-i.e., cTnI, as well as cTnT and cTnC-in viable but stunned peri-infarct tissue. In addition, we addressed the as-yet unexplored issue of whether the profound reduction of infarct size evoked by brief preconditioning ischemia (PC) was accompanied by a favorable attenuation in ischemia/reperfusion-induced degradation of cTnI, cTnT or cTnC in the remaining viable subepicardium. METHODS: Anesthetized open-chest dogs received 10 min of PC ischemia or a comparable control period, followed by 1 h of sustained coronary occlusion and 3 h of reperfusion. Subepicardial biopsies from the center of the soon-to-be ischemic territory were obtained at baseline and at 30 min and 3 h post-reflow, and myofilament protein integrity (intact cTnI, cTnT and cTnC, as well as degradation bands and covalent complexes) were assessed by Western immunoblotting. In addition, in all dogs, wall thickening was measured by echocardiography, collateral blood flow was assessed during sustained occlusion by injection of radiolabeled microspheres, and infarct size was delineated by tetrazolium staining. RESULTS: Although PC was, as expected, cardioprotective (infarct size of 2 +/- 1% of the risk region vs. 17 +/- 6% in controls; p < 0.05), both control and PC groups exhibited profound and comparable contractile dysfunction following reflow (mean wall thickening reduced to 20-22% of baseline values). There was, however, no significant degradation of cTnI in the viable but stunned, peri-infarct tissue. We did observe degradation of cTnT in the stunned subepicardium, an effect that was attenuated in dogs that received antecedent PC ischemia. However, there was no correlation between post-ischemic wall thickening and the immunoreactivity of the intact cTnT band, or wall thickening and the intensity of the cTnT degradation products. CONCLUSIONS: Our results suggest cTnI degradation is not a universal determinant of post-ischemic myocardial stunning. Moreover, the dissociation between cTnT degradation and wall thickening argue against a direct 'cause-and-effect' relationship between proteolysis of cTnT and acute, post-ischemic contractile dysfunction of stunned peri-infarct myocardium. Copyright 2004 European Society of Cardiology

Author information

Author/s: Colantonio, David A (DA); Van Eyk, Jennifer E (JE); Przyklenk, Karin (K);

Affiliation: Department of Physiology, Queen's University, Kingston, Ontario, Canada.

Journal and publication information

Publication Type: Journal Article

Journal: Cardiovascular research (Cardiovasc Res), published in Netherlands. (Language: eng)

Reference: 2004-Aug; vol 63 (issue 2) : pp 217-25

Dates: Created 2004/07/13; Completed 2004/10/13;

PMID: 15249179, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

Comments and Corrections

CommentIn: Cardiovasc Res. 2004 Aug 1;63(2):189-91. (PMID: 15249174)

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Blotting, Western - methods Dogs Echocardiography Models, Animal Myocardial Ischemia - metabolism

Myocardial Ischemia - metabolism Myocardial Stunning - metabolism; ultrasonography Myocardium - metabolism Troponin C - analysis; metabolism Troponin I - analysis; metabolism Troponin T - analysis; metabolism

Associated Chemicals: Troponin C (0) ; Troponin I (0) ; Troponin T (0)

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