Vascular reactivity is increased in rat lungs injured with alpha-naphthylthiourea.
Vascular reactivity is increased in rat lungs injured with alpha-naphthylthiourea.
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α-萘基硫脲损伤的大鼠肺部的血管反应性增加。
DOI：
10.1152/jappl.1983.54.6.1693
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Rounds,S
中科院分区：
文献类型：
--
作者：
Hill,NS;Rounds,S
我们研究了α-萘基硫脲（ANTU）所致肺损伤对肺血管反应性的影响。用ANTU（10 mg/kg ip）或溶剂吐温80处理大鼠。4小时后，ANTU治疗大鼠的肺湿干重比、支气管灌洗液蛋白浓度和血管周围水肿增加。为了测试血管反应性，分离肺并以恒定流速用血液灌注，同时监测平均肺动脉压。ANTU处理的肺血管收缩早于吐温处理的肺，以响应严重的气道缺氧（吸入O2分数0%）。ANTU处理的肺对10%O2的反应是血管收缩，而吐温处理的肺对10%O2没有反应，这表明ANTU降低了缺氧性血管收缩的阈值。ANTU还降低了血管紧张素II升压反应的阈值，并增加了血管紧张素II升压反应的幅度，表明血管反应性的增加不是缺氧所特有的。在灌注液中加入甲氨蝶呤可增加吐温处理肺对0%O2的反应速率和幅度，但不会改变ANTU处理肺的反应。ANTU处理的肺的光学显微镜显示没有肺动脉阻塞，和电子显微镜显示轻度毛细血管内皮细胞损伤。我们的结论是，增强肺血管反应性伴随着增加渗透性肺水肿所造成的ANTU。在成人呼吸窘迫综合征患者中观察到的血管反应性的类似增加可能有助于肺动脉高压。
We investigated the effects of lung injury due to alpha-naphthylthiourea (ANTU) on pulmonary vascular reactivity. Rats were treated with ANTU (10 mg/kg ip) or the vehicle Tween 80. Four hours later, lungs from ANTU-treated rats had increased wet-to-dry weight ratios, bronchial lavage protein concentrations, and perivascular edema. To test vascular reactivity, lungs were isolated and perfused with blood at constant flow rate, while mean pulmonary arterial pressure was monitored. ANTU-treated lungs vasoconstricted earlier than Tween-treated lungs in response to severe airway hypoxia (fractional inspired O2 0%). ANTU-treated lungs vasoconstricted in response to 10% O2, while Tween-treated lungs failed to respond to 10% O2, indicating that the threshold for hypoxic vasoconstriction was decreased by ANTU. ANTU also decreased the threshold for and increased the magnitude of angiotensin II pressor responses, indicating that the increased vasoreactivity was not specific for hypoxia. Addition of meclofenamate to perfusates increased the rate and magnitude of responses to 0% O2 in Tween-treated lungs, but did not change the responses of ANTU-treated lungs. Light microscopy of ANTU-treated lungs showed no pulmonary arterial obstruction, and electron microscopy revealed mild capillary endothelial cell injury. We conclude that enhanced pulmonary vascular reactivity accompanies the increased-permeability pulmonary edema caused by ANTU. A similar increase in vasoreactivity might contribute to pulmonary hypertension observed in patients with the adult respiratory distress syndrome.