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

David A. Colantonio, Jennifer E. Van Eyk, Karin Przyklenk

Research output: Contribution to journalArticle

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

Original languageEnglish (US)
Pages (from-to)217-225
Number of pages9
JournalCardiovascular Research
Volume63
Issue number2
DOIs
StatePublished - Aug 1 2004
Externally publishedYes

Fingerprint

Troponin T
Troponin I
Canidae
Myocardium
Ischemia
Reperfusion
Dogs
Myocardial Stunning
Troponin
Myofibrils
Coronary Occlusion
Microspheres
Echocardiography
Necrosis
Thorax
Western Blotting
Staining and Labeling
Biopsy
Injections
Proteins

Keywords

  • Peri-infarct myocardium
  • Troponin I
  • Troponin T

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Stunned peri-infarct canine myocardium is characterized by degradation of troponin T, not troponin I. / Colantonio, David A.; Van Eyk, Jennifer E.; Przyklenk, Karin.

In: Cardiovascular Research, Vol. 63, No. 2, 01.08.2004, p. 217-225.

Research output: Contribution to journalArticle

Colantonio, David A. ; Van Eyk, Jennifer E. ; Przyklenk, Karin. / Stunned peri-infarct canine myocardium is characterized by degradation of troponin T, not troponin I. In: Cardiovascular Research. 2004 ; Vol. 63, No. 2. pp. 217-225.
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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",
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AB - 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

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