rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    title: C-reactive protein impairs coronary microvascular function
    sub title: a dissertation
  name:
    name part: Qamirani, Erion.
    role:
      role term: creator
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2007
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: print
    extent: viii, 99 leaves : illustrations ; 28 cm.
  abstract: ABSTRACT: Elevated levels of C-reactive protein (CRP), a pro-inflammatory marker, are associated with reduced systemic endothelium-dependent nitric oxide (NO)-mediated dilation in patients with coronary artery disease; however, the direct effect of CRP on coronary microvascular reacticity remains unknown. Herein, we examined whether CRP can modulate endothelium-dependent vasodilatory pathways, and whether pro-inflammatory signaling pathways such as stress-activated protein kinases (p38 and JNK) and oxidative stress are involved in the CRP-mediated effect. Porcine coronary arterioles were isolated and pressurized without flow for in vitro study. Intraluminal treatment with a clinically relevant concentration of CRP (7 ug/mL, 1 hour) significantly attenuated the NO release and vasodilation to serotonin. Further incubation with the NO precursor L-arginine partially restored serotonin-induced vasodilation. The detrimental effect of CRP on serotonin-induced dilation was prevented in the presence of the superoxide scavenger TEMPOL, the NAD(P)H oxidase inhibitor apocynin, or the p38 kinase (an upstream activator of NAD(P)H oxidase) inhibitor SB203850, but not the xanthine oxidase inhibitor allopurinol or the c-Jun N-terminal kinase inhibitor SP600125. Dihydroethidium staining showed that CRP produced SB203850- and TEMPOL-sensitive superoxide production in the arteriolar endothelium. CRP treatment of coronary arterioles significantly increased NAD(P)H oxidase activity. Intraluminal treatment with CRP also attenuated endothelium-dependent, protacyclin (PGI₂)-mediated dilation to arachidonic acid (AA) and inhibited PGI₂ release from coronary microvessels. However, CRP did not affect endothelium-derived hyperpolarizing factor (EDHF)-mediated dilation to bradykinin. Scavenging peroxynitrite (a byproduct of superoxide and NO) with urate prevented the effect of CRP on the PGI₂-mediated dilation and PGI₂ release. LOX-1 receptor blockade with its antagonist k-carrageenan and LOX-1 …
  note: by Erion Qamirani.
  note: Vita.
  note: "Major Subject: Medical Sciences".
  note: "Submitted to the Graduate School of Biomedical Sciences of The Texas A&M University System Health Science Center in partial fulfillment for the requirements for the degree of Doctor of Philosophy May 2007."
  note: Approved as to style and content by: Lih Kuo, Michael Davis, Travis Hein, Emily Wilson, Harris Granger.
  note: Ph. D. Texas A&M University System Health Science Center 2007.
  note: Includes bibliographical references (leaves 83-98).
  subject:
    topic: Major Medical Sciences
  subject:
    topic: C-Reactive Protein
  subject:
    topic: Coronary Disease
  classification: W 4 AT4 Q11c 2007
  record info:
    record content source: TMV
    record creation date: 071211
    record change date: 20191204153055.0
    record identifier: in00004506334