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Transient venular permeability increase and endothelial gap formation induced by histamine
1Department of Physiology, College of Medicine, University of Arizona, Tucson.
The American Journal of Physiology
|April 1, 1992
Summary
Histamine temporarily increases blood vessel permeability by creating gaps between endothelial cells. These gaps form and close rapidly, mirroring the transient nature of histamine
Area of Science:
- Vascular Biology
- Cell Biology
- Pharmacology
Background:
- Histamine is a known mediator that increases venule permeability.
- This increase in permeability is transient, lasting only minutes.
- The mechanism behind this transient permeability is not fully understood.
Purpose of the Study:
- To test the hypothesis that transient permeability increases are caused by transient endothelial gaps.
- To correlate the time course of permeability changes with the formation and closure of endothelial gaps.
Main Methods:
- Experiments were conducted on single rat mesenteric venules.
- Permeability changes to alpha-lactalbumin were measured during histamine suffusion.
- Endothelial gap formation was analyzed using electron microscopy.
Main Results:
- Histamine caused a transient, fivefold increase in permeability, peaking around 3 minutes.
- The fraction of endothelial gaps increased significantly, mirroring permeability changes.
- Permeability and gap formation followed similar temporal patterns.
Conclusions:
- The study supports the hypothesis linking histamine-induced permeability to transient endothelial gaps.
- Transient endothelial gaps are the primary mechanism for histamine's short-term effect on venule permeability.