Mattioli L, Zakheim R M, Mullis K, Molteni A
J Pediatr. 1975 Jul;87(1):97-101. doi: 10.1016/s0022-3476(75)80081-3.
Serum angiotensin-I-converting enzyme activity was found to be elevated in infants with idiopathic respiratory distress syndrome when compared with healthy premature infants, normal infants, and acutely ill full-term infants. Serum and lung CE activity has been found to be elevated in mice exposed to hypobaric alveolar hypoxia which also stimulated renal renin production. These findings suggest that alveolar hypoxia stimulates the renin-angiotensin-aldosterone system and this system may be involved in the response to the stress of IRDS.
与健康早产儿、正常婴儿以及患急性病的足月儿相比，发现患有特发性呼吸窘迫综合征（IRDS）的婴儿血清血管紧张素I转换酶活性升高。在暴露于低压性肺泡低氧环境的小鼠中，血清和肺中的CE活性也被发现升高，而这种环境也刺激了肾脏肾素的产生。这些发现表明，肺泡低氧刺激肾素-血管紧张素-醛固酮系统，并且该系统可能参与对IRDS应激的反应。
