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Venous endothelial damage produced by massive sticking and emigration of leukocytes
Insights
Surgical trauma causes white blood cells to invade canine veins by migrating through endothelial junctions. Lidocaine and neutropenia prevented this invasion, highlighting the role of white cells in vascular injury.
Area of Science:
- Vascular biology
- Cellular and molecular medicine
- Surgical pathology
Background:
- White blood cell adhesion and transmigration are critical in inflammatory and injury responses.
- Endothelial integrity is crucial for maintaining vascular homeostasis.
- Surgical trauma can initiate complex cellular events within blood vessels.
Purpose of the Study:
- To investigate the mechanism of white blood cell invasion into canine veins following surgical trauma.
- To identify factors influencing white blood cell migration and endothelial damage.
- To evaluate the efficacy of lidocaine and neutropenia in preventing white blood cell invasion.
Main Methods:
- Scanning and transmission electron microscopy were used to examine canine jugular and femoral veins.
- Surgical trauma and external vessel occlusion were employed to induce vascular changes.
- Lidocaine (Xylocaine) administration and vinblastine-induced neutropenia were used to modulate white blood cell activity.
- Veins were perfused with normal blood to assess the role of circulating cells.
Main Results:
- Large numbers of white blood cells adhered to vessel walls and migrated through endothelial intercellular junctions.
- Endothelial cell separation and desquamation occurred, exposing subendothelial structures.
- Lidocaine effectively blocked white blood cell invasion.
- White blood cell invasion occurred in lidocaine-treated dogs when veins were perfused with normal blood.
- Vinblastine-induced neutropenia prevented white blood cell invasion, but invasion occurred when veins were perfused with normal blood.
Conclusions:
- Surgical trauma, not direct vessel injury, initiates white blood cell invasion via endothelial junctions.
- Lidocaine inhibits white blood cell migration, suggesting a role in managing post-surgical vascular inflammation.
- Neutropenia prevents white blood cell invasion, confirming their essential role in this process.
- Circulating white blood cells are necessary for invasion, even when endothelial barriers are compromised.
Abstract:
A scanning and transmission electron microscope study of canine jugular and femoral veins revealed that large numbers of white cells adhered to the vessel walls, passed through the endothelial intercellular junctions and accumulated in pockets between the endothelium and basement membrane. This led to extensive separation and desquamation of endothelial cells with exposure of subendothelial structures in many areas. The white cell invasion was caused by surgical trauma to adjacent tissues (rather than to the vessel itself) followed by 1 or 7 minutes occlusion by pressure applied externally just below the areas of dissection. The invasion was blocked by lidocaine (Xylocaine), an agent known to inhibit white cell migration. However, white cell invasion occurred when veins in lidocaine-treated dogs were perfused with normal blood. No white cell invasion occurred in dogs made neutropenic with vinblastine but did occur when these veins were perfused with normal blood.