Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Lipid-soluble smoke particles damage endothelial cells and reduce endothelium-dependent dilatation in rat and man

Zhang, JY ; Cao, YX ; Xu, Cang-Bao LU and Edvinsson, Lars LU (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:
author
; ; and
organization
publishing date
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
2021-02-17 07:40:32
@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 &lt; 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 &gt; 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},
}