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囊性纤维化患者口服补充L-精氨酸:一项安慰剂对照研究。

Oral L-arginine supplementation in cystic fibrosis patients: a placebo-controlled study.

作者信息

Grasemann H, Grasemann C, Kurtz F, Tietze-Schillings G, Vester U, Ratjen F

机构信息

Children's Hospital, University of Essen, Hufeland Str. 55, D-45122 Essen, Germany.

出版信息

Eur Respir J. 2005 Jan;25(1):62-8. doi: 10.1183/09031936.04.00086104.

DOI:10.1183/09031936.04.00086104
PMID:15640324
Abstract

Exhaled nitric oxide (eNO) is decreased in cystic fibrosis (CF). The effect of oral L-arginine, the precursor of enzymatic nitric oxide (NO) formation, on airway NO in patients with CF was studied. In a pilot study, oral L-arginine was given in a single dose of 200 mg x kg(-1) body weight to eight healthy controls and eight CF patients. Subsequently, the same L-arginine dose was given to 10 patients with CF (five females) t.i.d. for 6 weeks in a randomised double-blind placebo-controlled crossover study. A single dose of oral L-arginine resulted in a 5.5-fold increase of L-arginine in plasma and a 1.3-fold increase of L-arginine in sputum after 2 h. Maximum eNO, within 3 h of L-arginine intake, increased significantly in both CF patients (5.4+/-2.1 ppb versus 8.3+/-3.5 ppb) and controls (18.0+/-8.1 ppb versus 26.4+/-12.3 ppb). Supplementation of L-arginine for 6 weeks resulted in a sustained increase in eNO compared to placebo (9.7+/-5.7 ppb versus 6.3+/-3.1 ppb). An effect of L-arginine supplementation on forced expiratory volume in one second was not observed. These data indicate that airway nitric oxide formation in cystic fibrosis patients can be augmented with oral L-arginine supplementation.

摘要

呼出一氧化氮(eNO)在囊性纤维化(CF)患者中减少。本研究探讨了一氧化氮(NO)酶促生成的前体——口服L-精氨酸对CF患者气道NO的影响。在一项初步研究中,给8名健康对照者和8名CF患者单次口服200 mg·kg⁻¹体重的L-精氨酸。随后,在一项随机双盲安慰剂对照交叉研究中,给10名CF患者(5名女性)每日3次给予相同剂量的L-精氨酸,持续6周。单次口服L-精氨酸2小时后,血浆中L-精氨酸增加5.5倍,痰液中L-精氨酸增加1.3倍。在摄入L-精氨酸后3小时内,CF患者(5.4±2.1 ppb对8.3±3.5 ppb)和对照者(18.0±8.1 ppb对26.4±12.3 ppb)的最大eNO均显著增加。与安慰剂相比,补充L-精氨酸6周导致eNO持续增加(9.7±5.7 ppb对6.3±3.1 ppb)。未观察到补充L-精氨酸对一秒用力呼气容积的影响。这些数据表明,口服补充L-精氨酸可增强囊性纤维化患者气道一氧化氮的生成。

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