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Differences in arterial and arteriolar endothelial structure during endotoxin shock
E T Sutton1, Z Zhou, C H Baker
1Department of Physiology and Biophysics, College of Medicine, University of South Florida, Tampa 33612.
Circulatory Shock
|October 1, 1993
Summary
Escherichia coli endotoxin (ENDT) severely damages femoral artery endothelium but largely spares arterioles. This suggests differential susceptibility of vascular beds to endotoxin-induced injury.
Area of Science:
- Vascular Biology
- Endotoxic Shock
- Microcirculation
Background:
- Previous studies suggest differential effects of endotoxin on arteries and arterioles.
- Endotoxin abolishes acetylcholine-induced relaxation in femoral arteries.
- Arteriolar dilation responses to endotoxin vary, with A1 reduced and A2/A3 unchanged.
Purpose of the Study:
- To investigate the ultrastructural changes in femoral arteries and cremaster muscle arterioles following Escherichia coli endotoxin infusion.
- To compare the anatomical and functional damage to endothelial cells in arteries versus arterioles.
Main Methods:
- Infusion of Escherichia coli endotoxin (ENDT) in rats.
- Ultrastructural evaluation of femoral artery and A1, A2, A3 arteriole tissue.
- Assessment of endothelial cell integrity at varying mean arterial pressures (MAP).
Main Results:
- Endotoxin caused progressive destruction of femoral artery endothelial cells, denuding the internal elastic lamina at lower MAPs.
- Arterioles (A1, A2, A3) exhibited minimal endothelial damage, with only increased vacuolation in A1.
- Arteriolar endothelium remained relatively intact and functional, contrasting sharply with femoral artery damage.
Conclusions:
- Femoral arteries are highly susceptible to endotoxin-induced endothelial damage.
- Arterioles in the rat cremaster muscle demonstrate significant resistance to endotoxin-mediated injury.
- Differential vulnerability of vascular segments to endotoxin may have implications for circulatory shock pathophysiology.