Lipid-soluble smoke particles damage endothelial cells and reduce endothelium-dependent dilatation in rat and man
(2006) In BMC Cardiovascular Disorders 6(3).- Abstract
- Background: Cigarette smoking is a strong risk factor for vascular disease and known to cause
dysfunction of the endothelium. However, the molecular mechanisms involved are still not fully
understood.
Methods: In order to reveal the direct effects of lipid-soluble smoke particles on the endothelium,
ring segments isolated from rat mesenteric arteries and human middle cerebral arteries (MCA)
obtained at autopsy were incubated for 6 to 48 hrs in the presence of dimethylsulphoxide (DMSO)-
soluble particles from cigarette smoke (DSP), i.e. lipid-soluble smoke particles. The endothelial
microstructure was examined by transmission electron microscopy. The endothelial function... (More) - Background: Cigarette smoking is a strong risk factor for vascular disease and known to cause
dysfunction of the endothelium. However, the molecular mechanisms involved are still not fully
understood.
Methods: In order to reveal the direct effects of lipid-soluble smoke particles on the endothelium,
ring segments isolated from rat mesenteric arteries and human middle cerebral arteries (MCA)
obtained at autopsy were incubated for 6 to 48 hrs in the presence of dimethylsulphoxide (DMSO)-
soluble particles from cigarette smoke (DSP), i.e. lipid-soluble smoke particles. The endothelial
microstructure was examined by transmission electron microscopy. The endothelial function was
evaluated by acetylcholine (ACh)-induced endothelium-dependent vasodilatation, using a sensitive
myograph.
Results: After DSP treatment, the arterial endothelium was swollen and loosing its attachment. In
functional tests, the total ACh-induced dilatation, the nitric oxide (NO)-mediated and the
endothelium-derived hyperpolarization factor (EDHF)-mediated dilatations were significantly
decreased by DSP in a time- and concentration-dependent manner (p < 0.05). Nicotine, an
important compound in cigarette smoke had, in an equivalent concentration as in DSP, no such
effects (p > 0.05). Similar results were obtained in the human MCA.
Conclusion: Thus, we demonstrate that the lipid-soluble smoke particles, but not nicotine, caused
damage to arterial endothelium and reduced the endothelium-dependent dilatation in man and rat. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1137025
- author
- Zhang, JY ; Cao, YX ; Xu, Cang-Bao LU and Edvinsson, Lars LU
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- in
- BMC Cardiovascular Disorders
- volume
- 6
- issue
- 3
- publisher
- BioMed Central (BMC)
- external identifiers
-
- scopus:33644763047
- ISSN
- 1471-2261
- DOI
- 10.1186/1471-2261-6-3
- language
- English
- LU publication?
- yes
- id
- da1f2560-c5b5-448e-9026-b9f543bf5ab4 (old id 1137025)
- date added to LUP
- 2016-04-01 15:27:08
- date last changed
- 2024-02-09 07:22:55
@article{da1f2560-c5b5-448e-9026-b9f543bf5ab4,
abstract = {{Background: Cigarette smoking is a strong risk factor for vascular disease and known to cause<br/><br>
dysfunction of the endothelium. However, the molecular mechanisms involved are still not fully<br/><br>
understood.<br/><br>
Methods: In order to reveal the direct effects of lipid-soluble smoke particles on the endothelium,<br/><br>
ring segments isolated from rat mesenteric arteries and human middle cerebral arteries (MCA)<br/><br>
obtained at autopsy were incubated for 6 to 48 hrs in the presence of dimethylsulphoxide (DMSO)-<br/><br>
soluble particles from cigarette smoke (DSP), i.e. lipid-soluble smoke particles. The endothelial<br/><br>
microstructure was examined by transmission electron microscopy. The endothelial function was<br/><br>
evaluated by acetylcholine (ACh)-induced endothelium-dependent vasodilatation, using a sensitive<br/><br>
myograph.<br/><br>
Results: After DSP treatment, the arterial endothelium was swollen and loosing its attachment. In<br/><br>
functional tests, the total ACh-induced dilatation, the nitric oxide (NO)-mediated and the<br/><br>
endothelium-derived hyperpolarization factor (EDHF)-mediated dilatations were significantly<br/><br>
decreased by DSP in a time- and concentration-dependent manner (p < 0.05). Nicotine, an<br/><br>
important compound in cigarette smoke had, in an equivalent concentration as in DSP, no such<br/><br>
effects (p > 0.05). Similar results were obtained in the human MCA.<br/><br>
Conclusion: Thus, we demonstrate that the lipid-soluble smoke particles, but not nicotine, caused<br/><br>
damage to arterial endothelium and reduced the endothelium-dependent dilatation in man and rat.}},
author = {{Zhang, JY and Cao, YX and Xu, Cang-Bao and Edvinsson, Lars}},
issn = {{1471-2261}},
language = {{eng}},
number = {{3}},
publisher = {{BioMed Central (BMC)}},
series = {{BMC Cardiovascular Disorders}},
title = {{Lipid-soluble smoke particles damage endothelial cells and reduce endothelium-dependent dilatation in rat and man}},
url = {{http://dx.doi.org/10.1186/1471-2261-6-3}},
doi = {{10.1186/1471-2261-6-3}},
volume = {{6}},
year = {{2006}},
}