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肺水肿是多种疾病损害肺毛细血管上皮的的结果。在该处有丰富的血管紧张素转化酶(angiotensionconverting enzyme,ACE);ACE 的释放能反映肺脏受损伤的严重程度。因此,测定 ACE 的活性可作为临床有价值的辅助诊断及动物实验性肺损害毒理学的辅助指标。将硫脲注入鼠的体内,诱发肺水肿后,分别测定血清、肺脏灌洗液、胸腔渗出液内 ACE 的含量。给药后1小时,血清及肺灌洗液 ACE 升高。肺灌洗液ACE 升高,至少持续3小时;但此时血清含量已减少。胸腔渗出液中 ACE 的升高比肺灌洗液晚1小时,并能持续4小时之久。4小时后胸腔渗出液 ACE 总量可为0～90U。另一实验是测定肺内总的 ACE 值,作者发现在给药后1小时,当血清中 ACE 达峰值的同时,而在肺内总 ACE 含量则减少1,200U。作者指出,硫脲诱发急性肺损伤后,血清及肺灌
Pulmonary edema is the result of many diseases that damage the pulmonary capillary epithelium. There is an abundance of angiotensin converting enzyme (ACE); the release of ACE reflects the severity of lung damage. Therefore, the determination of ACE activity can be used as a clinically valuable adjuvant diagnostic and animal experimental lung injury toxicology auxiliary indicators. Thiourea was injected into the body of mice to induce pulmonary edema, respectively, serum, lung lavage fluid, pleural effusion ACE content. One hour after the administration, the serum and lung lavage fluid ACE increased. Pulmonary lavage fluid ACE increased for at least 3 hours; but serum levels have decreased at this time. ACE in thoracic exudates increased 1 hour later than lung lavage and sustained for 4 hours. 4 hours after pleural effusion ACE total amount of 0 ~ 90U. Another experiment was to determine the total ACE in the lung. The authors found that at 1 hour after administration, ACE peaked in the serum while total ACE was reduced by 1,200 U in the lung. The authors point out that thiourea-induced acute lung injury after serum and lung irrigation