Nitric oxide inhalation decreases pulmonary artery remodeling in the injured lungs of rat pups.
Nitric oxide inhalation decreases pulmonary artery remodeling in the injured lungs of rat pups.
复制标题
吸入一氧化氮可减少幼鼠受伤肺部的肺动脉重塑。
DOI：
10.1161/01.res.87.2.140
复制
发表时间：
2000
影响因子：
20.1
通讯作者：
Bloch,KD
中科院分区：
文献类型：
--
作者：
RobertsJr,JD;Chiche,JD;Weimann,J;Steudel,W;Zapol,WM;Bloch,KD
- 血管损伤导致外周肺动脉肌化，这在婴儿中比在成人肺中更明显。虽然吸入NO气体减轻缺氧大鼠肺动脉重构，但其是否通过减轻血管收缩来保护肺尚不清楚。本研究测试了吸入NO是否通过调节血管张力来降低大鼠幼仔损伤肺动脉的肌化。野百合碱给药后一周，肌化大鼠幼仔肺动脉的百分比增加>3倍。然而，野百合碱暴露并不引起右心室肥大，肺动脉高压，或血管收缩。此外，它没有增加炎症标志物（白细胞介素-1 β、细胞间粘附分子-1和E-选择素）或血小板介导的血栓形成（GPIbα）的表达。持续吸入20 ppm NO气体可防止肺损伤幼鼠肺动脉新生肌形成。此外，3倍的细胞增殖增加和细胞数量减少30%，在肺动脉野百合碱暴露所造成的NO吸入预防。这些数据表明，吸入NO通过独立于肺张力、炎症或血栓形成的机制保护婴儿免受肺损伤诱导的肺重塑。(Circ Res. 2000;87：140-145）。
—Vascular injury causes the muscularization of peripheral pulmonary arteries, which is more pronounced in the infant than in the adult lung. Although inhaled NO gas attenuates pulmonary artery remodeling in hypoxic rats, whether or not it protects the lung by mitigating vasoconstriction is unknown. This investigation tested whether inhaled NO decreases the muscularization of injured pulmonary arteries in rat pups by modulating vascular tone. One week after monocrotaline administration, the percentage of muscularized rat pup lung arteries was increased by >3-fold. Nevertheless, monocrotaline exposure did not cause right ventricular hypertrophy, pulmonary hypertension, or vasoconstriction. In addition, it did not increase the expression of markers of inflammation (interleukin-1β, intercellular adhesion molecule-1, and E-selectin) or of platelet-mediated thrombosis (GPIbα). Continuous inhalation of 20 ppm NO gas prevented the neomuscularization of the pulmonary arteries in pups with lung injury. Moreover, a 3-fold increase in cell proliferation and 30% decrease in cell numbers in pulmonary arteries caused by monocrotaline exposure was prevented by NO inhalation. These data indicate that inhaled NO protects infants against pulmonary remodeling induced by lung injury by mechanisms that are independent of pulmonary tone, inflammation, or thrombosis. (Circ Res. 2000;87:140-145.)