Title of article :
Endogenous nitric oxide in patients with chronic heart failure (CHF): relation to functional impairment and nitrate-containing therapies
Author/Authors :
Enrico Clini، نويسنده , , Maurizio Volterrani، نويسنده , , Marco Pagani، نويسنده , , Luca Bianchi، نويسنده , , Roberto Porta، نويسنده , , Lucia Sonia Gile’، نويسنده , , Amerigo Giordano، نويسنده , , Nicolino Ambrosino، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2000
Pages :
8
From page :
123
To page :
130
Abstract :
We assessed the levels of exhaled nitric oxide (eNO) in patients with chronic heart failure (CHF) according to the functional impairment and the use of nitrate-containing agents. Forty patients (age 55±9 years) were classified according to the NYHA classes I–II (n=18, group 1) and classes III–IV (n=22, group 2), and to the use of nitrate-containing drugs (Nitrate+, Nitrate−). Twenty-two healthy age-related subjects served as controls (group 3). Respiratory function, symptom-limited incremental cycloergometry and resting eNO concentration at peak (FENOp) or plateau (FENOpl) of the single-breath exhalation curve were assessed in all subjects. FENOpl was significantly lower in patients than in controls (7.8±2.7 and 10.6±2.8 ppb, respectively, P<0.005) and lower in most severe CHF patients (7.1±2.6 and 8.8±2.7 ppb in group 2 and group 1, respectively, P<0.05). A significant correlation between peak V′O2, Watts and FENOpl (r=0.42, P<0.013 and r=0.46, P=0.008, respectively) was found. Independent of NYHA class, Nitrate+ showed higher FENOp levels than Nitrate− patients (36.9±15.7 vs. 28.1±15.1 ppb, P<0.05). Resting eNO was lower in the most compromised CHF patients and was significantly related to exercise capacity. Nitrate-containing agents might influence the levels of eNO in these patients.
Keywords :
Nitric oxide , pulmonary hypertension , NO donors , chronic heart failure
Journal title :
International Journal of Cardiology
Serial Year :
2000
Journal title :
International Journal of Cardiology
Record number :
813095
Link To Document :
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