Hsu K, Huang K L, Wang D, Hsu C S, Chiang C H
Department of Medicine, Tri-Service General Hospital, Taipei, Taiwan, Republic of China.
Aviat Space Environ Med. 1997 Sep;68(9):802-6.
Venous gas bubbles are routinely detected in astronauts undergoing extravehicular activities at lower suit pressure. Venous air embolism increases the pulmonary arterial pressure and the vascular permeability leading to acute lung injury. In the present study we evaluated the protective effect of dibutyryl cAMP, aminophylline, and pentoxifylline on the pulmonary vasculatures after air embolism.
In isolated and perfused rat lungs, we induced air embolism by introducing air bubbles into the pulmonary artery. We measured the pulmonary arterial pressures and capillary pressure. Vascular permeability was determined by measuring the filtration coefficient (Kf) and the protein concentration in the lung lavage fluid.
Air infusion caused pulmonary hypertension and increased vascular permeability, resulting in pulmonary edema. The Kf (in g.min-1.cm H2O-1.100 g-1) increased from 0.44 +/- 0.05 at baseline to 2.98 +/- 0.47 after air infusion. Pretreatment with DBcAMP prevented the increase in Kf (0.63 +/- 0.09) caused by air embolism without altering the hemodynamics. Aminophylline and pentoxifylline did not prevent lung injury induced by air embolism. Although aminophylline did not alter the response of pulmonary arterial pressure to air infusion, it elevated the capillary pressure to 5.1 +/- 0.4 mmHg, which was significantly greater than that in the lung receiving air infusion alone.
Our results suggest that DBcAMP prevents the increase in vascular permeability caused air embolism. The ineffectiveness of aminophylline and pentoxifylline on the prevention of air embolism-induced lung injury remains for further investigation.
在舱外活动且航天服压力较低的宇航员中，经常能检测到静脉气泡。静脉空气栓塞会增加肺动脉压力和血管通透性，从而导致急性肺损伤。在本研究中，我们评估了二丁酰环磷腺苷、氨茶碱和己酮可可碱对空气栓塞后肺血管的保护作用。
在离体灌注的大鼠肺中，通过向肺动脉内注入气泡诱导空气栓塞。我们测量了肺动脉压力和毛细血管压力。通过测量滤过系数（Kf）和肺灌洗液中的蛋白质浓度来确定血管通透性。
注入空气导致肺动脉高压并增加血管通透性，进而引起肺水肿。Kf（单位：g·min⁻¹·cm H₂O⁻¹·100 g⁻¹）从基线时的0.44±0.05增加到注入空气后的2.98±0.47。用二丁酰环磷腺苷预处理可防止空气栓塞引起的Kf增加（0.63±0.09），且不改变血流动力学。氨茶碱和己酮可可碱不能预防空气栓塞引起的肺损伤。尽管氨茶碱没有改变肺动脉压力对注入空气的反应，但它使毛细血管压力升高至5.1±0.4 mmHg，这明显高于仅接受空气注入的肺中的压力。
我们的结果表明，二丁酰环磷腺苷可防止空气栓塞引起的血管通透性增加。氨茶碱和己酮可可碱在预防空气栓塞诱导的肺损伤方面无效，这仍有待进一步研究。
