An animal model of chronic coronary stenosis resulting in hibernating myocardium

H. Bolukoglu, A. J. Liedtke, S. H. Nellis, A. M. Eggleston, R. Subramanian, B. Renstrom

Research output: Contribution to journalArticle

71 Citations (Scopus)

Abstract

An experimental animal model of hibernating myocardium is presented. Sixteen animals were initially prepared of which seven were selected for final review. Hearts were instrumented in two separate surgical procedures such that maximum phasic flow velocity in the left anterior descending (LAD) coronary artery was reduced by 50% and followed over 1 wk. Regional shortening declined at 1 wk to 62% of aerobic values (P < 0.048) and did not improve over 2 h reperfusion. Metabolic determinations, obtained after 1 wk of coronary stenosis and immediately sampled before and after release of the LAD flow constrictor, showed no evidence of acidosis, hypercarbia, or an inability to extract oxygen at the tissue level. Thereafter, during the 2-h reperfusion period, hearts were able to respond to dobutamine (10 μg/kg infusion over 1 min) challenge with an appropriate shift in an endsystolic length estimate of contractility. Mitochondrial respiration at the conclusion of the studies in the reperfused bed demonstrated near normal recovery compared with aerobic values. None of the seven hearts showed gross evidence of infarction and only one heart was noted to have a few microfocal changes of healing infarction. Thus a new model of coronary stenosis is presented, which affected substantial reductions in mechanical function consistent with the concepts of hibernating myocardium. These mechanical events were not associated with marked metabolic abnormalities, reflecting advanced ischemia or mitochondrial dysfunction and could be transiently improved with inotropic stimuli. This model may prove beneficial as a tool in understanding mechanistic events underlying the hibernating heart.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume263
Issue number1 32-1
StatePublished - Jan 1 1992

Fingerprint

Coronary Stenosis
Myocardium
Animal Models
Infarction
Reperfusion
Dobutamine
Hypercapnia
Acidosis
Coronary Vessels
Respiration
Ischemia
Oxygen

Keywords

  • dobutamine challenge
  • mechanical dysfunction
  • mitochondrial respiration
  • reactive hyperemia

ASJC Scopus subject areas

  • Physiology

Cite this

Bolukoglu, H., Liedtke, A. J., Nellis, S. H., Eggleston, A. M., Subramanian, R., & Renstrom, B. (1992). An animal model of chronic coronary stenosis resulting in hibernating myocardium. American Journal of Physiology - Heart and Circulatory Physiology, 263(1 32-1).

An animal model of chronic coronary stenosis resulting in hibernating myocardium. / Bolukoglu, H.; Liedtke, A. J.; Nellis, S. H.; Eggleston, A. M.; Subramanian, R.; Renstrom, B.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 263, No. 1 32-1, 01.01.1992.

Research output: Contribution to journalArticle

Bolukoglu, H, Liedtke, AJ, Nellis, SH, Eggleston, AM, Subramanian, R & Renstrom, B 1992, 'An animal model of chronic coronary stenosis resulting in hibernating myocardium', American Journal of Physiology - Heart and Circulatory Physiology, vol. 263, no. 1 32-1.
Bolukoglu H, Liedtke AJ, Nellis SH, Eggleston AM, Subramanian R, Renstrom B. An animal model of chronic coronary stenosis resulting in hibernating myocardium. American Journal of Physiology - Heart and Circulatory Physiology. 1992 Jan 1;263(1 32-1).
Bolukoglu, H. ; Liedtke, A. J. ; Nellis, S. H. ; Eggleston, A. M. ; Subramanian, R. ; Renstrom, B. / An animal model of chronic coronary stenosis resulting in hibernating myocardium. In: American Journal of Physiology - Heart and Circulatory Physiology. 1992 ; Vol. 263, No. 1 32-1.
@article{d7146c5f32b84e67a063d3d22cd8d544,
title = "An animal model of chronic coronary stenosis resulting in hibernating myocardium",
abstract = "An experimental animal model of hibernating myocardium is presented. Sixteen animals were initially prepared of which seven were selected for final review. Hearts were instrumented in two separate surgical procedures such that maximum phasic flow velocity in the left anterior descending (LAD) coronary artery was reduced by 50{\%} and followed over 1 wk. Regional shortening declined at 1 wk to 62{\%} of aerobic values (P < 0.048) and did not improve over 2 h reperfusion. Metabolic determinations, obtained after 1 wk of coronary stenosis and immediately sampled before and after release of the LAD flow constrictor, showed no evidence of acidosis, hypercarbia, or an inability to extract oxygen at the tissue level. Thereafter, during the 2-h reperfusion period, hearts were able to respond to dobutamine (10 μg/kg infusion over 1 min) challenge with an appropriate shift in an endsystolic length estimate of contractility. Mitochondrial respiration at the conclusion of the studies in the reperfused bed demonstrated near normal recovery compared with aerobic values. None of the seven hearts showed gross evidence of infarction and only one heart was noted to have a few microfocal changes of healing infarction. Thus a new model of coronary stenosis is presented, which affected substantial reductions in mechanical function consistent with the concepts of hibernating myocardium. These mechanical events were not associated with marked metabolic abnormalities, reflecting advanced ischemia or mitochondrial dysfunction and could be transiently improved with inotropic stimuli. This model may prove beneficial as a tool in understanding mechanistic events underlying the hibernating heart.",
keywords = "dobutamine challenge, mechanical dysfunction, mitochondrial respiration, reactive hyperemia",
author = "H. Bolukoglu and Liedtke, {A. J.} and Nellis, {S. H.} and Eggleston, {A. M.} and R. Subramanian and B. Renstrom",
year = "1992",
month = "1",
day = "1",
language = "English (US)",
volume = "263",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "1 32-1",

}

TY - JOUR

T1 - An animal model of chronic coronary stenosis resulting in hibernating myocardium

AU - Bolukoglu, H.

AU - Liedtke, A. J.

AU - Nellis, S. H.

AU - Eggleston, A. M.

AU - Subramanian, R.

AU - Renstrom, B.

PY - 1992/1/1

Y1 - 1992/1/1

N2 - An experimental animal model of hibernating myocardium is presented. Sixteen animals were initially prepared of which seven were selected for final review. Hearts were instrumented in two separate surgical procedures such that maximum phasic flow velocity in the left anterior descending (LAD) coronary artery was reduced by 50% and followed over 1 wk. Regional shortening declined at 1 wk to 62% of aerobic values (P < 0.048) and did not improve over 2 h reperfusion. Metabolic determinations, obtained after 1 wk of coronary stenosis and immediately sampled before and after release of the LAD flow constrictor, showed no evidence of acidosis, hypercarbia, or an inability to extract oxygen at the tissue level. Thereafter, during the 2-h reperfusion period, hearts were able to respond to dobutamine (10 μg/kg infusion over 1 min) challenge with an appropriate shift in an endsystolic length estimate of contractility. Mitochondrial respiration at the conclusion of the studies in the reperfused bed demonstrated near normal recovery compared with aerobic values. None of the seven hearts showed gross evidence of infarction and only one heart was noted to have a few microfocal changes of healing infarction. Thus a new model of coronary stenosis is presented, which affected substantial reductions in mechanical function consistent with the concepts of hibernating myocardium. These mechanical events were not associated with marked metabolic abnormalities, reflecting advanced ischemia or mitochondrial dysfunction and could be transiently improved with inotropic stimuli. This model may prove beneficial as a tool in understanding mechanistic events underlying the hibernating heart.

AB - An experimental animal model of hibernating myocardium is presented. Sixteen animals were initially prepared of which seven were selected for final review. Hearts were instrumented in two separate surgical procedures such that maximum phasic flow velocity in the left anterior descending (LAD) coronary artery was reduced by 50% and followed over 1 wk. Regional shortening declined at 1 wk to 62% of aerobic values (P < 0.048) and did not improve over 2 h reperfusion. Metabolic determinations, obtained after 1 wk of coronary stenosis and immediately sampled before and after release of the LAD flow constrictor, showed no evidence of acidosis, hypercarbia, or an inability to extract oxygen at the tissue level. Thereafter, during the 2-h reperfusion period, hearts were able to respond to dobutamine (10 μg/kg infusion over 1 min) challenge with an appropriate shift in an endsystolic length estimate of contractility. Mitochondrial respiration at the conclusion of the studies in the reperfused bed demonstrated near normal recovery compared with aerobic values. None of the seven hearts showed gross evidence of infarction and only one heart was noted to have a few microfocal changes of healing infarction. Thus a new model of coronary stenosis is presented, which affected substantial reductions in mechanical function consistent with the concepts of hibernating myocardium. These mechanical events were not associated with marked metabolic abnormalities, reflecting advanced ischemia or mitochondrial dysfunction and could be transiently improved with inotropic stimuli. This model may prove beneficial as a tool in understanding mechanistic events underlying the hibernating heart.

KW - dobutamine challenge

KW - mechanical dysfunction

KW - mitochondrial respiration

KW - reactive hyperemia

UR - http://www.scopus.com/inward/record.url?scp=0026655462&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026655462&partnerID=8YFLogxK

M3 - Article

VL - 263

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 1 32-1

ER -