Related Experiment Video
Updated: Jul 17, 2026
05:47
A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision
Published on: May 13, 2021
Diesel exhaust particles induce endothelial dysfunction in apoE-/- mice
Christian S Hansen1, Majid Sheykhzade, Peter Møller
1Department of Environmental and Occupational Health, Institute of Public Health, University of Copenhagen, Øster Farimagsgade 5, Building 5B, 2nd Floor, 1014 Copenhagen K, Denmark.
Toxicology and Applied Pharmacology
|January 20, 2007
Summary
Diesel exhaust particles (DEP) acutely impair vascular function, particularly in mice with atherosclerosis. This suggests DEP exposure can induce endothelial dysfunction, potentially linked to nitric oxide (NO) pathways.
Area of Science:
- Environmental Health
- Cardiovascular Physiology
- Toxicology
Background:
- Particulate air pollution exacerbates cardiovascular disease.
- Mechanisms may involve particle translocation and endothelial dysfunction, influenced by atherosclerosis.
Purpose of the Study:
- Investigate diesel exhaust particle (DEP) effects on vasomotor function.
- Compare effects in atherosclerosis-prone (apoE(-/-)) and normal (apoE(+/+)) mice.
Main Methods:
- Administered DEP (0, 0.5, 5 mg/kg) intraperitoneally to mice.
- Measured vasomotor function in isolated aorta segments ex vivo.
- Incubated aorta segments with DEP (0, 10, 100 microg/ml) ex vivo.
Main Results:
- In vivo DEP (0.5 mg/kg) reduced vasorelaxation in apoE(-/-) mice but enhanced it in apoE(+/+) mice.
- DEP exposure did not alter constrictions to K+ or phenylephrine in vivo.
- Ex vivo DEP enhanced acetylcholine-induced relaxation and attenuated phenylephrine constriction.
Conclusions:
- DEP exposure has acute effects on vascular function.
- Endothelial dysfunction, possibly via reduced nitric oxide (NO) production, is induced by DEP in vivo, specifically in mice with existing atherosclerosis.
