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Journal of applied physiology (Bethesda, Md. : 1985)2005; 99(1); 224-229; doi: 10.1152/japplphysiol.01230.2004

Intrapulmonary arteriovenous shunts of >15 microm in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses.

Abstract: The present study examined whether Thoroughbred horses performing strenuous exercise exhibit intrapulmonary arteriovenous shunting that may contribute to the observed arterial hypoxemia. Experiments were carried out on seven healthy, exercise-trained Thoroughbreds at rest, maximal exercise (galloping at 14 m/s on a 3.5% uphill grade for 120 s), and submaximal exertion (8 m/s on a 3.5% uphill grade for 150 s). Along with blood gas/hemodynamic parameters, intrapulmonary arteriovenous shunting was studied by injecting 15-microm-diameter microspheres, labeled with different stable isotopes, into the right atrium while simultaneous blood samples were being withdrawn at a constant rate from the pulmonary artery and the aorta. Arterial hypoxemia was observed only during maximal exercise. Also, despite significant pulmonary arterial hypertension during submaximal and maximal exertion, 15-microm microspheres did not traverse the pulmonary microcirculation to appear in the aortic blood. Thus our findings did not support a role for intrapulmonary arteriovenous shunts of >15 microm in diameter in the exercise-induced arterial hypoxemia in racehorses. Interestingly, our observation that, in going from 30 to 120 s of maximal exertion, arterial O2 tension had remained unchanged despite significant reductions in mixed venous blood O2 tension, hemoglobin-O2 saturation, and O2 content also discounts the importance of intrapulmonary arteriovenous shunts in causing arterial hypoxemia. This is because, assuming that a constant fraction of total pulmonary blood flow bypasses the gas-exchange areas of the equine lungs via intrapulmonary arteriovenous shunts during 30-120 s of maximal exertion, the observed significant reductions in mixed venous blood oxygenation should cause a significant reduction in arterial O2 tension, which was not the case in our horses. Thus it is suggested that intrapulmonary arteriovenous shunting probably does not contribute to the exercise-induced arterial hypoxemia in racehorses.
Publication Date: 2005-03-17 PubMed ID: 15774703DOI: 10.1152/japplphysiol.01230.2004Google Scholar: Lookup
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Summary

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The research investigates if intrapulmonary arteriovenous shunting in Thoroughbred horses during strenuous exercise contributes to arterial hypoxemia – lower than normal levels of oxygen in the blood. The study concludes that larger arteriovenous shunts, above 15 micrometers in diameter, are likely not a factor in exercise-induced arterial hypoxemia in racing horses.

Study Design and Experiments

  • The study was conducted on seven healthy, exercise-trained Thoroughbred horses.
  • Experiments were executed at rest, at maximal exertion (sprinting at 14 meters per second uphill at a 3.5% slope) for two minutes, and at submaximal effort (running at 8 meters per second uphill at the same slope) for 150 seconds.
  • Through injection of differently labeled 15-microm microspheres into the right atrium, the research team monitored the degrees of intrapulmonary arteriovenous shunting. These microspheres were tracked all through the horse’s circulatory system allowing researchers to measure any shunting.
  • Simultaneous withdrawal and an examination of blood samples from the pulmonary artery and the aorta were performed to measure blood gas and hemodynamics.

Findings

  • Arterial hypoxemia was only observed during maximal exercise in the horses.
  • Even with significant pulmonary arterial hypertension during both submaximal and maximal exertion, the 15-microm microspheres did not appear in the aortic blood implying they did not cross the pulmonary microcirculation.
  • The finding did not support any role of intrapulmonary arteriovenous shunts larger than 15 microm in exercise-induced arterial hypoxemia in racehorses.

Further Observations

  • Interestingly, during maximum effort, arterial O2 tension didn’t change from 30 seconds to 120 seconds of activity even with significant drops in mixed venous blood oxygen, hemoglobin-O2 saturation, and O2 content.
  • This led to further rejecting the idea that arteriovenous shunts are a cause of arterial hypoxemia.
  • The researchers stated that if arteriovenous shunts were bypassing gas-exchange areas of the horse’s lungs during this time, there would be a decrease in arterial O2 tension due to reduced venous blood oxygenation, but this was not observed.

Conclusion

  • Intrapulmonary arteriovenous shunting likely does not contribute to exercise-induced arterial hypoxemia in racehorses.

Cite This Article

APA
Manohar M, Goetz TE. (2005). Intrapulmonary arteriovenous shunts of >15 microm in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses. J Appl Physiol (1985), 99(1), 224-229. https://doi.org/10.1152/japplphysiol.01230.2004

Publication

ISSN: 8750-7587
NlmUniqueID: 8502536
Country: United States
Language: English
Volume: 99
Issue: 1
Pages: 224-229

Researcher Affiliations

Manohar, Murli
  • Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, IL 61802, USA. mmanohar@uiuc.edu
Goetz, Thomas E

    MeSH Terms

    • Animals
    • Arteries / pathology
    • Arteries / physiopathology
    • Arteriovenous Anastomosis / pathology
    • Arteriovenous Anastomosis / physiopathology
    • Cross-Sectional Studies
    • Exercise Test
    • Female
    • Horse Diseases / pathology
    • Horse Diseases / physiopathology
    • Horses
    • Hypoxia / pathology
    • Hypoxia / physiopathology
    • Hypoxia / veterinary
    • Lung / blood supply
    • Lung / pathology
    • Lung / physiopathology
    • Male
    • Oxygen / metabolism
    • Physical Endurance
    • Pulmonary Circulation

    Citations

    This article has been cited 5 times.
    1. Lovering AT, Duke JW, Elliott JE. Intrapulmonary arteriovenous anastomoses in humans--response to exercise and the environment. J Physiol 2015 Feb 1;593(3):507-20.
      doi: 10.1113/jphysiol.2014.275495pubmed: 25565568google scholar: lookup
    2. Bates ML, Farrell ET, Drezdon A, Jacobson JE, Perlman SB, Eldridge MW. Hypoxia and exercise increase the transpulmonary passage of 99mTc-labeled albumin particles in humans. PLoS One 2014;9(7):e101146.
      doi: 10.1371/journal.pone.0101146pubmed: 25013985google scholar: lookup
    3. Lovering AT, Haverkamp HC, Romer LM, Hokanson JS, Eldridge MW. Transpulmonary passage of 99mTc macroaggregated albumin in healthy humans at rest and during maximal exercise. J Appl Physiol (1985) 2009 Jun;106(6):1986-92.
    4. Hopkins SR, Olfert IM, Wagner PD. Point: Exercise-induced intrapulmonary shunting is imaginary. J Appl Physiol (1985) 2009 Sep;107(3):993-4.
    5. Stickland MK, Lovering AT, Eldridge MW. Exercise-induced arteriovenous intrapulmonary shunting in dogs. Am J Respir Crit Care Med 2007 Aug 1;176(3):300-5.
      doi: 10.1164/rccm.200702-206OCpubmed: 17478619google scholar: lookup