title: Acute Chlamydia pneumoniae infection causes coronary endothelial dysfunction in pigs.
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.
  
  
  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 L-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 L-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. N(G)-nitro-L-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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Pediatric Cardiology, Lund University Hospital, Lund 22185, Sweden. petru.liuba@pedi.lu.se
authors.forename: Petru
authors.initials: P
authors.lastname: Liuba
authors.forename: Erkki
authors.initials: E
authors.lastname: Pesonen
authors.forename: Ilari
authors.initials: I
authors.lastname: Paakkari
authors.forename: Satish
authors.initials: S
authors.lastname: Batra
authors.forename: Anders
authors.initials: A
authors.lastname: Forslid
authors.forename: Petri
authors.initials: P
authors.lastname: Kovanen
authors.forename: Markku
authors.initials: M
authors.lastname: Pentikäinen
authors.forename: Kenneth
authors.initials: K
authors.lastname: Persson
authors.forename: Staffan
authors.initials: S
authors.lastname: Sandström
mesh_terms: D000208:Acute Disease; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001920:Bradykinin / Q000494:pharmacology; D023521:Chlamydophila Infections / Q000150:complications*; D016993:Chlamydophila pneumoniae; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000382:microbiology* / Q000473:pathology; D003331:Coronary Vessels / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000382:microbiology / Q000473:pathology* / Q000503:physiopathology; D005978:Glutathione / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D011336:Probability; D012016:Reference Values; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D001120:Arginine; D019001:Nitric Oxide Synthase; D005978:Glutathione; D001920:Bradykinin