Hales C A, Rouse E, Buchwald I A, Kazemi H
Respir Physiol. 1977 Apr;29(2):151-62. doi: 10.1016/0034-5687(77)90088-3.
The role of prostaglandins as mediators of alveolar hypoxic vasoconstriction was investigated in dogs with the use of the prostaglandin synthesis inhibitors, aspirin and indomethacin. Alveolar hypoxia was induced by inserting double-lumened endotracheal tube into the carina and ventilating one lung with nigrogen while maintaining normal systemic oxygenation with 100% O(2) ventilation to the other lung. Relative perfusion to each lung was determined with 133Xenon and external counters. Infusions up to 25 mg/kg of indomethacin and up to 250 mg/kg of aspirin did not block the shift in perfusion from the alveolar hypoxic lung. In fact, the shift in perfusion from the alveolar hypoxic lung was slightly augmented by aspirin (P = 0.03). Thus, no positive role was demonstrated in the dog for prostaglandins in producing the vasoconstriction of alveolar hypoxia.
使用前列腺素合成抑制剂阿司匹林和消炎痛,在犬身上研究了前列腺素作为肺泡低氧性血管收缩介质的作用。通过在隆突处插入双腔气管导管,用氮气对一侧肺进行通气,同时用100%氧气对另一侧肺进行通气以维持正常的全身氧合,从而诱导肺泡低氧。用133氙和外部计数器测定每侧肺的相对灌注。高达25mg/kg的消炎痛和高达250mg/kg的阿司匹林输注并未阻断灌注从肺泡低氧肺的转移。事实上,阿司匹林使灌注从肺泡低氧肺的转移略有增加(P = 0.03)。因此,在犬身上未证明前列腺素在产生肺泡低氧性血管收缩方面有积极作用。