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采用自行改良的肺血管通透性实验方法建立了黄嘌呤和黄嘌呤氧化酶（Ｘ－ＸＯ）所致肺血管通透性损伤大鼠动物模型，并研究了血管活性肠肽（ＶＩＰ）对其肺血管通透性损伤的调节作用。在含１ｍｍｏｌ／Ｌ黄嘌呤的生理缓冲液中加入０．０５Ｕ／ｍｌ黄嘌呤氧化酶进行闭合肺动脉重复灌注３０ｍｉｎ后测定￣（１２５）Ⅰ－白蛋白渗漏指数（￣（１２５）Ⅰ－ＡＬＩ）等参数。结果显示，气道压力尚无显著增加的情况下￣（１２５）Ⅰ－ＡＬＩ已有显著提高，３倍于正常对照组；其它生理学指标也出现不同程度的变化，即Ｘ－ＸＯ组（ｎ＝６）＞ＶＩＰ－Ｘ－ＸＯ组（ｎ＝６）＞正常对照组（ｎ＝６）。加入黄嘌呤氧化酶（ＸＯ）３０ｍｉｎ后肺灌注液中血栓素Ｂ＿２（ＴＸＢ＿２）和６－酮－前列腺素Ｆ＿（１α）（６－ｋｅｔｏ－ＰＧＦ＿（１α））均明显增高，但ＶＩＰ的前处理取消了这种反应。本实验结果表明肺血管通透性损伤可能是活性氧基引起急性肺水肿、急性呼吸窘迫综合征（ＡＲＤＳ）的重要原因，ＶＩＰ作为一种抗氧化剂神经肽起着保护肺血管通透性的作用。
The animal model of pulmonary vascular permeability injury induced by xanthine and xanthine oxidase (X-XO) was established by self-modified pulmonary vascular permeability test and the effects of vasoactive intestinal peptide (VIP) Pulmonary vascular permeability injury regulation. The 125I-albumin leakage index (~ (125) I-ALI) was determined by adding 0.05U / ml xanthine oxidase into the physiological buffer solution containing 1mmol / L xanthine for 30min after the closed pulmonary artery was reperfused for 30min. Other parameters. The results showed that ~ (125) Ⅰ-ALI had been significantly increased 3 times higher than that of the normal control group without any significant increase in airway pressure; other physiological indicators also changed to varying degrees, namely X-XO group (n = 6)> VIP-X-XO group (n = 6)> normal control group (n = 6). Thromboxane B 2 (TXB 2) and 6-keto-PGF 1α (6-keto-PGF_ (1α)) in lung perfusate were significantly increased after xanthine oxidase (XO) administration for 30 min, but VIP pretreatment Canceled this reaction. The experimental results show that pulmonary vascular permeability damage may be reactive oxygen species cause acute pulmonary edema, acute respiratory distress syndrome (ARDS) an important reason, VIP as an antioxidant neuropeptide plays a protective pulmonary vascular permeability .