Pulmonary capillary endothelial dysfunction in hypoxia and endotoxemia: A biochemical and electron microscope study

James M. Bisio, Roy E. Breen, Reid S. Connell, Marvin W. Harrison

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


The pulmonary capillary endothelial cell (PCEC) performs many hydrolytic and uptake functions directed toward removal or modification of circulating vasoactive substances. The present study utilized enzymatic hydrolysis of exogenous adenosine triphosphate (ATP) to quantitatively assess the integrity of the PCEC in rat lungs subjected to acute alveolar hypoxia and acute endotoxemia. Both of these experimental conditions produce gross, histologic, and electron microscopic changes that are similar to those associated with shock lung. Sixty-eight male Sprague-Dawley rats were used. In one group of animals acute alveolar hypoxia was induced for 2 hours by reducing the inspired oxygen concentration to 7%. The animals were then assayed for PCEC metabolic activity. In the second group of animals, 20 mg/kg E. coli endotoxin was administered intravenously and the animals were assayed for PCEC hydrolytic activity 4 or 24 hours later. In all animals, the heart and lungs were isolated and perfused with a buffer containing ATP. The amount of inorganic phosphorous (Pi) liberated after passage through the lungs was used as a marker for PCEC activity. In the group of animals given endotoxin, lungs of control animals liberated 0.173 ± 0.047 mg/cc/gm tissue Pi. Animals given endotoxin liberated 0.125 ± 0.071 mg/cc/gm tissue Pi at 4 hours (p < 0.05) and 0.121 ± 0.082 mg/cc/gm Pi at 24 hours (p < 0.05). In the hypoxic group, control animals liberated 0.170 ± 0.043 mg/cc/gm tissue Pi. Lungs of animals made hypoxic liberated 0.075 ± 0.041 mg/cc/gm tissue Pi (p < 0.001). Reduced levels of hydrolytic activity corresponded with the degree of ultrastructural disruption in lungs of animals subjected to hypoxia or endotoxemia. This assay is a reliable and reproducible measure of cellular damage occurring with stresses known to produce pulmonary insufficiency. By using this method, we attempted to evaluate quantitatively the efficacy of therapeutic intervention aimed at prevention of respiratory distress following shock.

Original languageEnglish (US)
Pages (from-to)730-739
Number of pages10
JournalJournal of Trauma - Injury, Infection and Critical Care
Issue number8
StatePublished - Aug 1983
Externally publishedYes

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine


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