Uhlig S, Featherstone R L, Wilhelms O H, Wendel A
University of Konstanz, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1996 Nov;354(5):684-8. doi: 10.1007/BF00170846.
In the isolated perfused rat lung, perfusion with platelet-activating factor causes bronchoconstriction, vasoconstriction and edema formation. The bronchoconstriction and vasoconstriction are largely mediated by thromboxane, whereas the edema formation is due to enhanced vascular permeability unrelated to eicosanoids. Since natriuretic peptides are known to relax smooth muscle and were suggested to attenuate enhanced vascular permeability, we investigated the effect of urodilatin on the PAF-induced alterations in lung function. Pretreatment with urodilatin (0.25 microM or 0.75 microM) reduced the PAF-induced increase in airway and vascular resistance by approximately 50%. Urodilatin pretreatment, however, was completely ineffective against the PAF-induced increase in weight gain and in vascular permeability, as assessed by the vascular filtration coefficient. Furthermore, urodilatin failed to affect the release of thromboxane into the perfusate in PAF-exposed lungs. Thus, urodilatin relaxes airway and vascular smooth muscle, but fails to reduce edema formation in PAF-perfused rat lungs.
在离体灌注的大鼠肺中，用血小板活化因子灌注会导致支气管收缩、血管收缩和水肿形成。支气管收缩和血管收缩主要由血栓素介导，而水肿形成是由于与类二十烷酸无关的血管通透性增强所致。由于已知利钠肽可使平滑肌松弛，并有人提出其可减轻血管通透性增强，因此我们研究了尿舒张素对血小板活化因子诱导的肺功能改变的影响。用尿舒张素（0.25微摩尔或0.75微摩尔）预处理可使血小板活化因子诱导的气道和血管阻力增加降低约50%。然而，根据血管滤过系数评估，尿舒张素预处理对血小板活化因子诱导的体重增加和血管通透性增加完全无效。此外，尿舒张素未能影响血小板活化因子暴露的肺中血栓素释放到灌注液中。因此，尿舒张素可使气道和血管平滑肌松弛，但不能减轻血小板活化因子灌注的大鼠肺中的水肿形成。
