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Titolo:
L-arginine reduces heart rate and improves hemodynamics in severe congestive heart failure
Autore:
Bocchi, EA; de Moraes, AV; Esteves, A; Bacal, F; Auler, JO; Carmona, MJ; Bellotti, G; Ramires, AF;
Indirizzi:
Univ Sao Paulo, Sch Med, Inst Heart, Sao Paulo, Brazil Univ Sao Paulo SaoPaulo Brazil Sch Med, Inst Heart, Sao Paulo, Brazil
Titolo Testata:
CLINICAL CARDIOLOGY
fascicolo: 3, volume: 23, anno: 2000,
pagine: 205 - 210
SICI:
0160-9289(200003)23:3<205:LRHRAI>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
INHALED NITRIC-OXIDE; CARDIAC-MUSCLE; ENDOTHELIAL FUNCTION; VASODILATION; CORONARY; HUMANS; VASOCONSTRICTION; DISTENSIBILITY; CONTRACTILITY; PERFORMANCE;
Keywords:
nitric oxide; heart failure; L-arginine; endothelium-derived factors; left ventricular function;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Bocchi, EA Rua Oscar Freire 2077,Apto 161, BR-05409011 Sao Paulo, Brazil Rua Oscar Freire 2077,Apto 161 Sao Paulo Brazil BR-05409011 BC
Citazione:
E.A. Bocchi et al., "L-arginine reduces heart rate and improves hemodynamics in severe congestive heart failure", CLIN CARD, 23(3), 2000, pp. 205-210

Abstract

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 CHE acting through the nitric oxide (NO)-L-arginine pathway or by growth hormone increment. Hypothesis: 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 thefollowing parameters using echocardiography and an LV Millar Mikro-Tip catheter simultaneously under four conditions: basal. during NO inhalation (40ppm), 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 I ate (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 1/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. Conclusion: 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.

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Documento generato il 03/12/20 alle ore 21:54:40