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血管紧张素转换酶（ACE）已作为肺毛细血管内皮细胞受损的指示性指标，本研究旨在评价吸入一氧化氮（NO）对吸入性损伤后肺血管内皮细胞的影响。用21只犬随机分为3组，烟雾吸入后，吸氧组（n=8）单纯吸氧（FiO2，0．45）；NO治疗组（n=9）吸氧（FiO2，0．45）＋0．0045％（45PPm）NO，连续监测12小时动脉血ACE活性变化；正常组（n＝4）不致伤，用于建立组织学对照。动脉血数据行多个样本均数间方差分析，支气管肺泡灌洗液（BALF）和肺组织ACE活性行两样本均数t检验。结果治疗组血浆ACE活性比对照组降低（P＜0．05）；BALF和肺组织中，治疗组ACE活性也明显低于对照组（P＜0．01）。吸入NO对犬烟雾吸入性损伤肺毛细血管内皮细胞有一定减轻损害作用。
Angiotensin-converting enzyme (ACE) has been used as an indicator of impairment of pulmonary capillary endothelial cells. This study was designed to evaluate the effect of inhaled nitric oxide (NO) on pulmonary vascular endothelial cells after inhalation injury. Twenty-one dogs were randomly divided into three groups. After inhalation of smoke, oxygen (FiO2, 0.45) in the oxygen inhalation group (n = 8) and FiO2 (0.45) +0.0045% (45PPm) NO, continuous monitoring of changes in ACE activity 12 hours arterial blood; normal group (n = 4) not injury, for the establishment of histological control. Arterial blood samples were analyzed by ANOVA, bronchoalveolar lavage fluid (BALF), and ACE activity in lung tissue using two-sample mean t-test. Results The plasma ACE activity in treatment group was lower than that in control group (P <0.05). In BALF and lung tissue, ACE activity in treatment group was significantly lower than that in control group (P <0.01). Inhalation of NO on canine smoke inhalation injury pulmonary capillary endothelial cells have a certain lessening damage.