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Acute Chlamydia pneumoniae infection causes coronary endothelial dysfunction in pigs.

Liuba, Petru LU ; Pesonen, Erkki LU ; Paakkari, Ilari; Batra, Satish LU ; Forslid, Anders LU ; Kovanen, Petri; Pentikäinen, Markku; Persson, Kenneth LU and Sandström, Staffan LU (2003) In Atherosclerosis 167(2). p.215-222
Abstract
Background: Coronary endothelial dysfunction contributes to the pathogenesis of acute coronary syndromes (ACSs). Acute Chlamydia pneumoniae infection has been epidemiologically associated with ACS. In this study, we investigated whether acute C. pneumoniae infection could alter the endothelial vasomotor function of porcine coronary vessels. Methods and results: Twenty pigs, 7–9 kg in weight, were inoculated intratracheally with C. pneumoniae (n=12) or saline (n=8), and investigated at 3 days (five infected/four non-infected) and 2 weeks (5+2 infected/four non-infected) after inoculation. The endothelium-dependent reactivity of coronary microcirculation was assessed at both time points by measuring peak coronary flow velocity (CFV) in... (More)
Background: Coronary endothelial dysfunction contributes to the pathogenesis of acute coronary syndromes (ACSs). Acute Chlamydia pneumoniae infection has been epidemiologically associated with ACS. In this study, we investigated whether acute C. pneumoniae infection could alter the endothelial vasomotor function of porcine coronary vessels. Methods and results: Twenty pigs, 7–9 kg in weight, were inoculated intratracheally with C. pneumoniae (n=12) or saline (n=8), and investigated at 3 days (five infected/four non-infected) and 2 weeks (5+2 infected/four non-infected) after inoculation. The endothelium-dependent reactivity of coronary microcirculation was assessed at both time points by measuring peak coronary flow velocity (CFV) in response to bradykinin, before and after infusions with glutathione, an antioxidant, and Image-arginine, a substrate for nitric oxide synthase (NOS). CFV after bradykinin was significantly decreased in infected animals at both time points. At 2 weeks, both glutathione and Image-arginine significantly improved CFV after bradykinin. CFV after sodium nitroprusside (SNP) was similar in both groups. At 3 days, the relaxation responses of bradykinin-induced pre-contracted left anterior descending (LAD) coronary rings to bradykinin were significantly less in infected animals. NG-nitro-Image-arginine-methyl-ester, an NOS inhibitor, had significantly greater inhibitory effect on bradykinin-induced relaxation in infected animals. Plasma nitrate–nitrite and fibrinogen, and NOS activity from LAD coronary samples were significantly increased in infected animals. Conclusion: Acute C. pneumoniae infection causes endothelial dysfunction of both resistance and epicardial coronary vessels, and favours a pro-coagulant status. These effects could in part account for the epidemiologically suggested association between acute infection and ACS. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Acute infection, Endothelium, Coronary, Chlamydia pneumoniae
in
Atherosclerosis
volume
167
issue
2
pages
215 - 222
publisher
Elsevier
external identifiers
  • wos:000182343600005
  • pmid:12818403
  • scopus:0038801326
ISSN
1879-1484
DOI
10.1016/S0021-9150(03)00019-4
language
English
LU publication?
yes
id
a5deffad-3347-4bfd-a14f-6d33cfc5212f (old id 115788)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12818403&dopt=Abstract
date added to LUP
2007-06-26 11:01:55
date last changed
2018-02-18 03:43:40
@article{a5deffad-3347-4bfd-a14f-6d33cfc5212f,
  abstract     = {Background: Coronary endothelial dysfunction contributes to the pathogenesis of acute coronary syndromes (ACSs). Acute Chlamydia pneumoniae infection has been epidemiologically associated with ACS. In this study, we investigated whether acute C. pneumoniae infection could alter the endothelial vasomotor function of porcine coronary vessels. Methods and results: Twenty pigs, 7–9 kg in weight, were inoculated intratracheally with C. pneumoniae (n=12) or saline (n=8), and investigated at 3 days (five infected/four non-infected) and 2 weeks (5+2 infected/four non-infected) after inoculation. The endothelium-dependent reactivity of coronary microcirculation was assessed at both time points by measuring peak coronary flow velocity (CFV) in response to bradykinin, before and after infusions with glutathione, an antioxidant, and Image-arginine, a substrate for nitric oxide synthase (NOS). CFV after bradykinin was significantly decreased in infected animals at both time points. At 2 weeks, both glutathione and Image-arginine significantly improved CFV after bradykinin. CFV after sodium nitroprusside (SNP) was similar in both groups. At 3 days, the relaxation responses of bradykinin-induced pre-contracted left anterior descending (LAD) coronary rings to bradykinin were significantly less in infected animals. NG-nitro-Image-arginine-methyl-ester, an NOS inhibitor, had significantly greater inhibitory effect on bradykinin-induced relaxation in infected animals. Plasma nitrate–nitrite and fibrinogen, and NOS activity from LAD coronary samples were significantly increased in infected animals. Conclusion: Acute C. pneumoniae infection causes endothelial dysfunction of both resistance and epicardial coronary vessels, and favours a pro-coagulant status. These effects could in part account for the epidemiologically suggested association between acute infection and ACS.},
  author       = {Liuba, Petru and Pesonen, Erkki and Paakkari, Ilari and Batra, Satish and Forslid, Anders and Kovanen, Petri and Pentikäinen, Markku and Persson, Kenneth and Sandström, Staffan},
  issn         = {1879-1484},
  keyword      = {Acute infection,Endothelium,Coronary,Chlamydia pneumoniae},
  language     = {eng},
  number       = {2},
  pages        = {215--222},
  publisher    = {Elsevier},
  series       = {Atherosclerosis},
  title        = {Acute Chlamydia pneumoniae infection causes coronary endothelial dysfunction in pigs.},
  url          = {http://dx.doi.org/10.1016/S0021-9150(03)00019-4},
  volume       = {167},
  year         = {2003},
}