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Effects of endotoxin on lung water, hemodynamics, and gas exchange in anesthetized ponies.

Abstract: Effects of endotoxemia on lung water, hemodynamics, and gas exchange were determined in ponies breathing a mixture of halothane and 100% O2. Escherichia coli endotoxin was infused IV at 20 micrograms/kg of body weight for 1 hour followed by 10 micrograms/kg/hr the subsequent 4 hours. By 0.25 hour, endotoxin increased mean pulmonary artery pressure and pulmonary vascular resistance; this was followed by a return to base-line values by 0.5 and 1 hour, respectively. A 2nd increase in pulmonary vascular resistance occurred by 5 hours of endotoxemia. During the last 2 hours of endotoxin infusion, cardiac index was significantly (P less than 0.05) decreased. Hematocrit was increased from 1 to 5 hours of endotoxemia, whereas, the plasma protein concentration was increased from 2 to 4 hours, indicating a loss of plasma volume. The PaO2 and PaCO2 were unchanged. After 5 hours of endotoxemia, lung extravascular thermal volume, postmortem bronchoalveolar lavage albumin content, and extravascular lung water/extravascular dry weight ratio of bloodless lungs were not increased, indicating no increase in alveolar-capillary permeability or pulmonary edema.
Publication Date: 1985-11-01 PubMed ID: 3907435
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research investigates the effects of endotoxins on lung water, blood circulation, and gas exchange in ponies under anesthesia. The study observed that endotoxins cause considerable changes in mean pulmonary artery pressure, pulmonary vascular resistance, and cardiac index, ultimately leading to a loss of plasma volume, without necessarily increasing alveolar-capillary permeability or causing lung edema.

Methodology

  • The study was carried out on ponies that were administered with a mixture of halothane and 100% O2 to induce anesthesia.
  • The ponies were intravenously administered with Escherichia coli endotoxin. The dosage was 20 micrograms per kilogram of body weight for the first hour, which was then reduced to 10 micrograms per kilogram for the next four hours.

Results

  • Within the first quarter-hour, the endotoxin caused an increase in the mean pulmonary artery pressure and the pulmonary vascular resistance. Both parameters returned to their base-line values by the end of one hour.
  • A second spike in pulmonary vascular resistance was observed after five hours of endotoxemia.
  • In the last two hours of endotoxin infusion, the cardiac index recorded a significant decrease.
  • Hematocrit levels were increased between the first to the fifth hour of endotoxemia, suggesting a loss of plasma volume.
  • Plasma protein concentration also increased between the second and fourth hour, corroborating indication of plasma volume loss.
  • However, the PaO2 and PaCO2 levels remained stable despite these changes.
  • After five hours of endotoxemia, lung extravascular thermal volume, postmortem bronchoalveolar lavage albumin content, and the ratio of extravascular lung water to extravascular dry weight of bloodless lungs did not increase, indicating there was no increase in alveolar-capillary permeability or the presence of pulmonary edema.

Conclusion

  • Endotoxemia triggers notable changes in pulmonary artery pressure, vascular resistance, and cardiac index, potentially indicating a loss of plasma volume.
  • Despite these effects, endotoxins do not appear to contribute towards an increased alveolar-capillary permeability or cause pulmonary edema.

Cite This Article

APA
Olson NC. (1985). Effects of endotoxin on lung water, hemodynamics, and gas exchange in anesthetized ponies. Am J Vet Res, 46(11), 2288-2293.

Publication

ISSN: 0002-9645
NlmUniqueID: 0375011
Country: United States
Language: English
Volume: 46
Issue: 11
Pages: 2288-2293

Researcher Affiliations

Olson, N C

    MeSH Terms

    • Animals
    • Endotoxins / pharmacology
    • Escherichia coli
    • Hemodynamics / drug effects
    • Horse Diseases / chemically induced
    • Horses / physiology
    • Pulmonary Edema / chemically induced
    • Pulmonary Gas Exchange / drug effects

    Citations

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