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Lung microvessel injury from peritoneal abscesses and gram-negative bacteremia
1Department of Anesthesia, Massachusetts General Hospital-East, Charlestown.
Abstract:
To analyze the effect of an extrathoracic focus of infection on lung vessel wall structure, we produced peritoneal abscesses in the rat, over a period of 3 to 7 weeks, by implanting capsules containing live gram-negative bacteria (3.0 x 10(7) Escherichia coli and 5.0 x 10(7) Bactercides fragilis) with an adjutant. We document here by arteriography, morphometric analysis, and high resolution microscopy, microvessel cell injury, and wall remodeling. In the sepsis-injured lung, both dilated and thick-walled microvessels are present. The walls of dilated vessels are disrupted by extensive endothelial and precursor smooth muscle cell injury. In thick-walled vessels these cells are hypertrophied, and the precursor smooth muscle cells express filaments, demonstrating a shift toward a contractile phenotype. Infiltrating monocytic cells focally consolidate alveolar regions. In the residual nonconsolidated regions, alveolar-capillary membrane cells are attenuated and the capillaries dilated. Vessel changes after 7 weeks are similar to those after 3 weeks but alveolar-capillary membrane injury is more extensive. These structural changes, including the development of precursor smooth muscle cells, may contribute to the known increase in reactivity of these lung vessels to challenge by vasoactive agents.
Insights
Extrathoracic infection causes lung microvessel damage and remodeling in rats. These changes, including cell injury and smooth muscle development, may increase lung vessel reactivity.
Area of Science:
- Pulmonary Medicine
- Pathology
- Microbiology
Background:
- Extrathoracic infections can lead to systemic inflammation and affect distant organs.
- Lung microvascular structure and function are critical for gas exchange and can be altered during sepsis.
Purpose of the Study:
- To investigate the structural changes in lung microvessels resulting from a remote focus of infection (peritoneal abscess).
- To analyze the cellular and tissue remodeling within lung vasculature during sepsis.
Main Methods:
- Induction of peritoneal abscesses in rats using gram-negative bacteria (Escherichia coli and Bacteroides fragilis).
- Analysis of lung microvessels using arteriography, morphometric analysis, and high-resolution microscopy at 3 and 7 weeks post-induction.
- Evaluation of endothelial cells, smooth muscle cells, and alveolar-capillary membranes.
Main Results:
- Sepsis induced both dilated and thick-walled lung microvessels.
- Dilated vessels showed endothelial and smooth muscle cell injury, while thick-walled vessels exhibited hypertrophied cells with a shift towards a contractile phenotype.
- Alveolar-capillary membranes were attenuated and capillaries dilated in non-consolidated areas, with more extensive injury observed at 7 weeks.
Conclusions:
- Remote infections significantly alter lung microvessel structure, causing cell injury and remodeling.
- The development of precursor smooth muscle cells suggests a potential mechanism for increased lung vessel reactivity.
- These structural adaptations may contribute to altered pulmonary vascular responses during sepsis.