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Cold storage sensitizes rat femoral artery to an endotoxin-induced decrease in endothelium-dependent relaxation.

Harro A Piepot¹, Ioannis A Pneumatikos, A B Johan Groeneveld

¹Laboratory for Physiology, Institute of Cardiovascular Research, Free University Medical Center, Amsterdam, The Netherlands.

The Journal of Surgical Research

|July 18, 2002

Summary

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Cold storage sensitizes rat arteries to endotoxin, increasing vasoconstriction and decreasing relaxation. This explains why infections harm cold-stored arterial grafts and transplanted tissues.

Area of Science:

Vascular Surgery
Transplantation Medicine
Immunology

Background:

Cold-stored tissues and organs are vital for vascular, reconstructive, and transplantation surgeries.
Infections can compromise the function of transplanted vessels and tissues, increasing patient morbidity.

Purpose of the Study:

To investigate the effects of cold storage on basal vascular reactivity.
To assess how cold storage alters the sensitivity of arteries to endotoxin.

Main Methods:

Isolated rat femoral artery segments were used in a crossover design.
Vessels were exposed to endotoxin (Escherichia coli 0127:B8) or control solution before and after cold storage.
Vascular reactivity was measured using a wire myograph with KCl, norepinephrine, acetylcholine, and sodium nitroprusside.

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Main Results:

Cold storage alone did not affect vascular reactivity.
Endotoxin reduced norepinephrine response pre-storage and SNP sensitivity both pre- and post-storage.
Post-cold storage, endotoxin impaired acetylcholine-induced relaxation and enhanced KCl/norepinephrine vasoconstriction.

Conclusions:

Cold storage does not impair endothelial or smooth muscle function but sensitizes arteries to endotoxin.
This sensitization leads to reduced endothelium-dependent relaxation and increased vasoconstriction.
Findings suggest a mechanism for infection-related dysfunction in cold-stored arterial grafts and transplanted tissues.