PMID- 21806669
OWN - NLM
STAT- MEDLINE
DCOM- 20120131
LR  - 20131121
IS  - 1440-1681 (Electronic)
IS  - 0305-1870 (Linking)
VI  - 38
IP  - 10
DP  - 2011 Oct
TI  - Platelet activation, oxidative stress and overexpression of inducible nitric 
      oxide synthase in moderate heart failure.
PG  - 705-10
LID - 10.1111/j.1440-1681.2011.05580.x [doi]
AB  - 1. Chronic heart failure (CHF) is a common disabling disorder associated with 
      thromboembolic events, the genesis of which is not yet fully understood. Nitric 
      oxide (NO), derived from the vascular endothelium and platelets, has an important 
      role in the physiological regulation of blood flow. It is generated from the 
      amino acid L-arginine via NO synthase (NOS). 2. The main objective of the present 
      study was to investigate NO production and its relationship with platelet 
      aggregation, oxidative stress, inflammation and related amino acids in patients 
      with moderate CHF. The expression and activity of NOS isoforms were analysed by 
      western blotting and conversion of L-[(3)H]-arginine to L-[(3)H]-citrulline, 
      respectively, in CHF patients (n = 12) and healthy controls (n = 15). Collagen- 
      and ADP-induced platelet aggregation, oxidative stress (thiobarbituric 
      acid-reactive substances (TBARS) formation and superoxide dismutase (SOD) 
      activity) and plasma levels of amino acids and inflammatory markers (fibrinogen 
      and C-reactive protein (CRP)) were also determined. 3. Both collagen- and 
      ADP-induced platelet aggregation were increased in CHF patients compared with 
      controls. Platelets from CHF patients did not show any changes in NOS activity in 
      the presence of overexpression of inducible NOS. Systemic and intraplatelet TBARS 
      production was elevated, whereas SOD activity was decreased in CHF patients. 
      l-arginine plasma concentrations were lower in CHF patients than in controls. 
      Systemic levels of CRP and fibrinogen were increased in CHF patients. 4. The 
      results show that, in patients with moderate CHF, there is platelet activation 
      and reduced intraplatelet NO bioavailability due to oxidative stress, which 
      suggests a role for platelets in the prothrombotic state.
CI  - (c) 2011 The Authors. Clinical and Experimental Pharmacology and Physiology (c) 2011 
      Blackwell Publishing Asia Pty Ltd.
FAU - de Meirelles, Luisa R
AU  - de Meirelles LR
AD  - Departament of Pharmacology and Psychobiology, State University of Rio de 
      Janeiro, Rio de Janeiro, Brazil.
FAU - Resende, Angela de C
AU  - Resende Ade C
FAU - Matsuura, Cristiane
AU  - Matsuura C
FAU - Salgado, Angelo
AU  - Salgado A
FAU - Pereira, Natalia R
AU  - Pereira NR
FAU - Cascarelli, Pedro G
AU  - Cascarelli PG
FAU - Mendes-Ribeiro, Antonio C
AU  - Mendes-Ribeiro AC
FAU - Brunini, Tatiana M C
AU  - Brunini TM
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 61D2G4IYVH (Adenosine Diphosphate)
RN  - 9001-32-5 (Fibrinogen)
RN  - 9007-34-5 (Collagen)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Adenosine Diphosphate/pharmacology
MH  - Arginine/blood
MH  - Blood Platelets/metabolism/physiology
MH  - C-Reactive Protein/metabolism
MH  - Case-Control Studies
MH  - Collagen/pharmacology
MH  - Female
MH  - Fibrinogen/metabolism
MH  - Heart Failure/*metabolism/*physiopathology
MH  - Humans
MH  - Inflammation/metabolism
MH  - Male
MH  - Middle Aged
MH  - Nitric Oxide Synthase Type II/*metabolism
MH  - Nitric Oxide Synthase Type III/metabolism
MH  - Oxidative Stress/*physiology
MH  - Platelet Activation/*drug effects
MH  - Platelet Aggregation/drug effects/*physiology
MH  - Superoxide Dismutase/blood/metabolism
MH  - Thiobarbituric Acid Reactive Substances/metabolism
EDAT- 2011/08/03 06:00
MHDA- 2012/02/01 06:00
CRDT- 2011/08/03 06:00
PHST- 2011/08/03 06:00 [entrez]
PHST- 2011/08/03 06:00 [pubmed]
PHST- 2012/02/01 06:00 [medline]
AID - 10.1111/j.1440-1681.2011.05580.x [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 2011 Oct;38(10):705-10. doi: 
      10.1111/j.1440-1681.2011.05580.x.