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The American journal of physiology1996; 270(6 Pt 2); H1893-H1904; doi: 10.1152/ajpheart.1996.270.6.H1893

Equine coronary hemodynamics during brief coronary occlusions at three levels of collateral function.

Abstract: Adult-grade ponies were surgically instrumented with a Doppler flow probe and pneumatic cuff occluder on the left anterior descending coronary artery (LAD), sonomicrometry crystals and intraventricular micromanometer in the left ventricle, and catheters in the left atrium, anterior interventricular vein, and, in some animals, the LAD. Conscious-animal studies were begun 2 wk after surgery. Measured variables included regional left ventricular systolic function, end-diastolic wall thickness, oxygen extraction, lactate extraction, and hydrogen ion release. Changes in collateral perfusion were deduced from changes in these variables. Serial data were obtained during a 3-min LAD occlusion before stimulation of collateral function by the intermittent coronary occlusion method and during a 10-min LAD occlusion after 14 +/- 2 and 27 +/- 2 days of stimulation. Hemodynamic interpretation of data was based on a model of the equine coronary circulation consisting of collateral and arteriolar resistances in series. It was concluded that 1) chronic stimulation of collateral function leads to the emergence of a time-dependent reduction in total collateral resistance during acute coronary occlusion; 2) with enhancement of collateral function, the major resistance controlling collateral blood flow shifts from the collateral circulation to the recipient vessel arterioles; and 3) at a certain level of enhanced collateral function, coronary occlusion results in a triphasic blood flow response in collateral-dependent myocardium consisting of early hypoperfusion, transient hyperperfusion, and late autoregulated perfusion. This study demonstrates that chronic stimulation of collateral function is accompanied by specific alterations in coronary hemodynamics during acute coronary occlusion that hasten the recovery of ischemic myocardium.
Publication Date: 1996-06-11 PubMed ID: 8764237DOI: 10.1152/ajpheart.1996.270.6.H1893Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • U.S. Gov't
  • P.H.S.

Summary

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This research explores the effects of chronic stimulation of coronary collateral function in ponies on the hemodynamics of the heart during acute coronary occlusion. It demonstrated that such stimulation led to specific changes in blood flow dynamics that quickened the recovery of ischemic heart muscle.

Experiment Procedure

  • Adult ponies were surgically equipped with various instruments including a Doppler flow probe and pneumatic cuff occluder on the left anterior descending coronary artery (LAD), sonomicrometry crystals and an intraventricular micromanometer in the left ventricle, and catheters in the left atrium and anterior interventricular vein.
  • In some ponies, the LAD was also catheterised.
  • Two weeks post-surgery, studies were conducted on the conscious animals.

Variables Monitored

  • Different variables such as regional left ventricular systolic function, end-diastolic wall thickness, and lactate extraction were measured.
  • Levels of oxygen extraction and hydrogen ion release were also analysed.
  • Changes in collateral perfusion (alternate pathways for blood flow) were inferred from fluctuations in these variables.
  • Data were collected progressively during periods of LAD occlusion prior to and following collateral function stimulation via the intermittent coronary occlusion method.

Interpretation of Data

  • The researchers used a model of horse coronary circulation involving collateral and arteriolar resistances in series for data interpretation.
  • They deduced that chronic stimulation of collateral function causes a time-dependent decrease in the total collateral resistance during acute coronary occlusion.
  • Moreover, optimized collateral function shifts the main resistance controlling collateral blood flow from the collateral circulation to the recipient vessel arterioles.
  • At a certain threshold of enhanced collateral function, coronary occlusion elicits a three-phase blood flow reaction in the collateral-dependent myocardium, characterised by initial reduced perfusion, temporary hyperperfusion and later, autoregulated perfusion.

Key Findings and Implication

  • The study highlights that chronic stimulation of collateral function correlates with specific changes in blood flow patterns during acute coronary occlusion.
  • This process expedites the healing of ischemic myocardial tissue (heart muscle tissue that has experienced a lack of blood flow).

Cite This Article

APA
Williams DO, Boatwright RB, Rugh KS, Ross CR, Sarazan RD, Garner HE, Griggs DM. (1996). Equine coronary hemodynamics during brief coronary occlusions at three levels of collateral function. Am J Physiol, 270(6 Pt 2), H1893-H1904. https://doi.org/10.1152/ajpheart.1996.270.6.H1893

Publication

ISSN: 0002-9513
NlmUniqueID: 0370511
Country: United States
Language: English
Volume: 270
Issue: 6 Pt 2
Pages: H1893-H1904

Researcher Affiliations

Williams, D O
  • Department of Physiology, University of Missouri, Columbia 65211, USA.
Boatwright, R B
    Rugh, K S
      Ross, C R
        Sarazan, R D
          Garner, H E
            Griggs, D M

              MeSH Terms

              • Animals
              • Blood Pressure
              • Collateral Circulation
              • Coronary Circulation
              • Coronary Disease / physiopathology
              • Heart / physiopathology
              • Hemodynamics
              • Homeostasis
              • Horses
              • Myocardium / metabolism

              Grant Funding

              • F32-HL-06999 / NHLBI NIH HHS
              • F32-HL-07639 / NHLBI NIH HHS
              • R37-HL-11876 / NHLBI NIH HHS

              Citations

              This article has been cited 1 times.
              1. Weis R, Carstensen H, Sattler SM, Buhl R, Hesselkilde EM. Electrocardiographic Changes in a Horse with Induced Myocardial Infarction. Animals (Basel) 2022 May 16;12(10).
                doi: 10.3390/ani12101272pubmed: 35625118google scholar: lookup