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Related Experiment Videos

Endothelial cell dysfunction in microvasculature: relevance to disease processes.

M Oda1, J Y Han, M Nakamura

  • 1Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan. m-oda@med.keio.ac.jp

Clinical Hemorheology and Microcirculation
|April 26, 2001
PubMed
Summary

Microvascular endothelial cell (EC) changes trigger disease by disrupting microcirculation. Endotoxemia and stress alter ECs, leading to leukocyte extravasation and organ damage, as seen in gastric ulcers and liver cirrhosis.

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Area of Science:

  • Physiology
  • Pathology
  • Microcirculation Research

Background:

  • Microvascular endothelial cell (EC) dysfunction is central to microcirculatory disturbances and disease development.
  • Endotoxemia, common in severe diseases, can trigger microcirculatory disorders like disseminated intravascular coagulation (DIC) and multiple organ failure (MOF).
  • Stress-induced autonomic nerve overstimulation also impacts microvascular ECs, contributing to tissue injury.

Purpose of the Study:

  • To investigate the role of microvascular EC alterations in disease pathogenesis.
  • To explore the mechanisms by which endotoxemia and stress affect ECs and microcirculation.
  • To understand the ultrastructural changes in hepatic microvasculature during liver cirrhosis and endotoxemia.

Main Methods:

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  • Intravital microscopy in rats to observe microcirculation changes after endotoxin (LPS) infusion.
  • Vital staining with monastral blue B (MBB) to identify altered ECs.
  • Transmission electron microscopy (TEM) to examine EC morphology, actin filaments, and hepatic sinusoidal endothelial fenestrae (SEF).

    • Main Results:

    • LPS infusion induced a low flow state in rat mesenteric microcirculation, with MBB-positive ECs at postcapillary venules.
    • MBB-positive ECs showed contracted morphology, facilitating leukocyte and erythrocyte extravasation, similar to histamine-induced diapedesis.
    • Gastric mucosal microvessels exhibited EC alterations under stress, leading to diapedesis and injury. Liver cirrhosis showed reduced SEF and basement membrane formation, linked to endothelin-1 (ET-1).

    Conclusions:

    • Microvascular EC alterations, including contraction and fenestral changes, are critical in endotoxemia- and stress-induced microcirculatory disorders.
    • Leukocyte extravasation through altered ECs contributes to inflammatory responses and tissue damage in conditions like gastric ulcers.
    • ET-1 mediated changes in hepatic microvasculature contribute to portal hypertension and impaired endotoxin clearance in liver cirrhosis.