Pakbaz H, Berisha H, Sharaf H, Foda H D, Said S I
SUNY at Stony Brook.
Ann N Y Acad Sci. 1994 Jun 17;723:426-8.
VIP delayed the onset of edematous lung injury in isolated perfused rat lungs by 64%, and was more effective than PGI2 in prolonging lung survival ex vivo. While PGI2 increased survival by 37 min versus Krebs/BSA only, VIP increased it by 2 h and 17 min. On the other hand, inhibition of NO. synthase, which protected the lung against oxidant injury caused by paraquat or X/XO,3 actually hastened the onset of injury caused by prolonged perfusion ex vivo, suggesting opposite roles for NO. in different forms of oxidant injury.
血管活性肠肽（VIP）使离体灌注大鼠肺水肿性肺损伤的发生延迟了64%，并且在延长肺离体存活时间方面比前列环素（PGI2）更有效。与仅使用 Krebs/牛血清白蛋白（BSA）相比，PGI2使存活时间增加了37分钟，而VIP使存活时间增加了2小时17分钟。另一方面，抑制一氧化氮（NO）合酶，它可保护肺免受百草枯或黄嘌呤/黄嘌呤氧化酶（X/XO）引起的氧化损伤，实际上却加速了离体长时间灌注所致损伤的发生，这表明NO在不同形式的氧化损伤中发挥着相反的作用。
