L-arginine reduces heart rate and improves hemodynamics in severe congestive heart failure.
BACKGROUND
Stimulated endothelium-derived relaxing factor-mediated vasodilation and conduit artery distensibility are impaired in congestive heart failure (CHF). L-arginine could have a potentially beneficial role in CHF, acting through the nitric oxide (NO)-L-arginine pathway or by growth hormone increment.


OBJECTIVE
This study was undertaken to investigate the effects of L-arginine on heart rate, hemodynamics, and left ventricular (LV) function in CHF.


METHODS
In seven patients (aged 39 +/- 8 years) with CHF, we obtained the following parameters using echocardiography and an LV Millar Mikro-Tip catheter simultaneously under four conditions: basal, during NO inhalation (40 ppm), in basal condition before L-arginine infusion, and after L-arginine intravenous infusion (mean dose 30.4 +/- 1.9 g).


RESULTS
Nitric oxide inhalation increased pulmonary capillary wedge pressure from 25 +/- 9 to 31 +/- 7 mmHg (p < 0.05), but did not change echocardiographic variables or LV contractility by elastance determination. L-arginine decreased heart rate (from 88 +/- 15 to 80 +/- 16 beats/min, p<0.005), mean systemic arterial pressure (from 84 +/- 17 to 70 +/- 18 mmHg, p < 0.007), and systemic vascular resistance (from 24 +/- 8 to 15 +/- 6 Wood units, p<0.003). L-arginine increased right atrial pressure (from 7 +/- 2 to 10 +/- 3 mmHg, p<0.04), cardiac output (from 3.4 +/- 0.7 to 4.1 +/- 0.8 l/min, p < 0.009), and stroke volume (from 40 +/- 9 to 54 +/- 14 ml, p < 0.008). The ratios of pulmonary vascular resistance to systemic vascular resistance at baseline and during NO inhalation were 0.09 and 0.075, respectively, and with L-arginine this increased from 0.09 to 0.12.


CONCLUSIONS
L-arginine exerted no effect on contractility; however, by acting on systemic vascular resistance it improved cardiac performance. L-arginine showed a negative chronotropic effect. The possible beneficial effect of L-arginine on reversing endothelial dysfunction in CHF without changing LV contractility should be the subject of further investigations.
Bocchi
E A
EA
Heart Institute, Medical School of São Paulo University, Brazil.
Vilella de Moraes
A V
AV
Esteves-Filho
A
A
Bacal
F
F
Auler
J O
JO
Carmona
M J
MJ
Bellotti
G
G
Ramires
A F
AF
D000328:Adult; D001120:Arginine / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007262:Infusions, Intravenous; D008875:Middle Aged; D009569:Nitric Oxide / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*
D014665:Vasodilator Agents; D009569:Nitric Oxide; D001120:Arginine