PMID- 14668566
OWN - NLM
STAT- MEDLINE
DCOM- 20040413
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 43
IP  - 1
DP  - 2004 Jan
TI  - Coxsackievirus B3 infection compromises endothelial-dependent vasodilation of 
      coronary resistance arteries.
PG  - 39-47
AB  - The mechanisms of coronary artery dysfunction in coxsackievirus B3 
      (CVB3)-mediated viral myocarditis are poorly understood. We used pressure 
      myography of mouse septal coronary arteries to determine the early and late 
      effects of CVB3 infection on vascular function. Male CD-1 mice (age 6-7 weeks) 
      were infected with CVB3 (1.75 x 10(10) pfu, i.p.). Control mice were injected 
      with PBS. Mice were killed at 3, 7, and 42 days post infection, and the 
      ventricular septal artery was dissected and mounted on a pressure myograph. 
      Pressure-induced myogenic tone was similar in CVB3-infected and sham-infected 
      mice at 3 and 7 days post infection. However, at 42 days post infection 
      constriction of septal arteries to pressures equal to or less than 60 mm Hg was 
      enhanced in CVB3-infected mice compared with sham controls. Agonist-induced 
      vasodilation, as assessed by response to acetylcholine (1 nM-3 microM), was 
      unaltered at early time points (days 3 and 7) in CVB3-infected mice. At later 
      time points (day 42), there was a significant decrease in ACh-induced 
      vasodilation in CVB3-infected mice. Bosentan, an ET-1 (ETA and ETB) receptor 
      antagonist, did not completely ameliorate the reduced ACh-induced vasodilation in 
      42-day infected mice, indicating that ET-1 does not contribute to vascular 
      dysfunction. Smooth muscle function, as measured by constriction to KCl or 
      dilation to sodium nitroprusside, was unchanged in infected mice at early and 
      late time points. Immunohistochemistry and ET-1 immunoassay were then performed 
      to assess ET-1 levels in CVB3- and sham-infected hearts. There were no 
      differences in ET-1 protein localization or levels at 42 days post infection in 
      sham- and CVB3-infected animals. Finally, in situ hybridization and TUNEL 
      staining were performed to assess viral localization and cell death in 
      CVB3-infected hearts. There was no detectable CVB3 or TUNEL positivity in the 
      endothelium of coronary arteries. Therefore, late impairment of 
      endothelial-dependent vasorelaxation of coronary resistance vessels in 
      CVB3-induced myocarditis does not appear to involve altered ET-1 expression but 
      may be secondary to decreased stimulated NO secretion by the endothelium.
FAU - Choy, Jonathan C
AU  - Choy JC
AD  - UBC McDonald Research Laboratories/The iCAPTUR4E Centre, Department of Pathology 
      and Laboratory Medicine, St. Paul's Hospital/Providence Health Care-University of 
      British Columbia, British Columbia, Canada.
FAU - Lui, Amy H
AU  - Lui AH
FAU - Moien-Afshari, Farzad
AU  - Moien-Afshari F
FAU - Wei, Kevin
AU  - Wei K
FAU - Yanagawa, Bobby
AU  - Yanagawa B
FAU - McManus, Bruce M
AU  - McManus BM
FAU - Laher, Ismail
AU  - Laher I
LA  - eng
GR  - K08-HL03909/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Endothelin-1)
RN  - 0 (Sulfonamides)
RN  - 0 (Vasodilator Agents)
RN  - N9YNS0M02X (Acetylcholine)
RN  - Q326023R30 (Bosentan)
SB  - IM
MH  - Acetylcholine/pharmacology
MH  - Animals
MH  - Antihypertensive Agents/pharmacology
MH  - Bosentan
MH  - Coronary Vessels/*physiopathology
MH  - Coxsackievirus Infections/*physiopathology
MH  - Endothelin-1/metabolism
MH  - Endothelium, Vascular/*metabolism
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Mice
MH  - Models, Cardiovascular
MH  - Myocarditis/*physiopathology
MH  - Sulfonamides/pharmacology
MH  - Vasodilation/drug effects
MH  - Vasodilator Agents/pharmacology
EDAT- 2003/12/12 05:00
MHDA- 2004/04/14 05:00
CRDT- 2003/12/12 05:00
PHST- 2003/12/12 05:00 [pubmed]
PHST- 2004/04/14 05:00 [medline]
PHST- 2003/12/12 05:00 [entrez]
AID - 10.1097/00005344-200401000-00007 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 2004 Jan;43(1):39-47. doi: 
      10.1097/00005344-200401000-00007.