【作者】 王金勇；

【导师】 王小龙；

【作者基本信息】 南京农业大学 ， 临床兽医学， 2000， 硕士

【摘要】 本文分别采用饮水高钠和低温环境下日粮中添加T₃的方法诱发肉鸡肺动脉高压综合征，通过右心导管法直接测定肺动脉压及测定血浆一氧化氮（nitric oxide，NO）含量等方法，研究了一氧化氮供体、前体物质及一氧化氮合酶抑制剂对肉鸡肺动脉压及肺动脉高压综合征发病率的影响。结果如下： 试验一中，饮水高钠导致肉鸡肺动脉压显著升高（p＜0.01），静注硝普钠后高钠组和对照组肉鸡血浆NO水平显著升高（p＜0.01），肺动脉平均压（mean pulmonary arterial pressure，mPAP）都显著降低（p＜0.01），高钠组肉鸡mPAP降压幅度高于对照组（p＜0.05）。表明硝普钠可通过释放一氧化氮降低肉鸡肺动脉平均压； 在试验二、三、四中可见如下结果，低温同时添加T₃处理后试验组肉鸡mPAP升高，腹水综合征发病率增加，红细胞压积、右心全心比及血浆T₃、血浆内皮素（endothelin-1，ET-1）水平与对照组相比都显著升高，mPAP变化与血浆ET-1含量变化之间存在明显正相关，两组肉鸡血浆NO水平差异不显著，但都出现随日龄增加血浆NO水平升高现象；日粮添加精氨酸后，血浆NO水平升高，肉鸡腹水发生率明显降低，肺动脉高压和右心肥大的出现的比未添加精氨酸肉鸡延迟一周；日粮添加一氧化氮合酶抑制剂L-NAME进一步增加了低温同时添加T₃处理诱发的腹水综合征发病率，右心肥大的出现比不加L-NAME组提前一周。 试验五中，静注L-NAME1-2小时后肉鸡血浆NO含量降低（P＜0.05），肺动脉压升高（P＜0.05）。静注L-NAME4小时后肉鸡血浆NO含量回升，肺动脉压回落至正常水平。 上述结果提示，一氧化氮合成增加可能抑制了肉鸡肺动脉高压的形成，降低了腹水综合征发病率；一氧化氮合成减少则可能促进了肺动脉高压的形成和腹水综合征的发生。更多还原

【Abstract】 Pulmonary hypertension syndrome in broilers was induced by twoways: high sodium concentration in drinking water and low temperature coped with 1.5 ppm 3,3,5-triiodothyronine (T3) supplemented dietary, and effect of nitric oxide (NO) on pulmonary arterial pressure and ascites morbidity in broilers were observed. The experimental results were as following: In experiment 1, high sodium concentration in drinking water increased mean pulmonary arterial pressure (mPAP) , Sodium Nitroprusside (SNP), a kind of donor of NO, intravenously infusion reduced mPAP from 25.96 ?2.96 mmHg to 18.39?.69 mmHg (p<O.Ol) by releasingNO. In experiment 2 3 4, dietary 13 and low temperature significantly increased ascites morbidity , mPAP ~. PCV RV/TV and values of plasma ET- 1 and 13. Plasma El-i and mPAP had a significant correlation (r=0.726). No significant difference was found in plasma NO of two groups, but the trend of increasement of plasma NO with the days delaying was observed. Ascites morbidity was reduced by L-arginine (substrate of NO) supplemented to diet and the forming of pulmonary hypertension and right ventricular hypertrophy was delayed one week along with the increase of plasma NO. Ascites morbidity was further increased by L-NAME (nitric oxide synthase inhibitor) supplemented to diet and the forming of right ventricular hypertrophy was one week early than low temperature group without L-NAME. In experiment 4, In the first 1 -2h after intravenously infusion of L-NAME, The was mPAP increased from 20.0?.49 mmHg to 24.25-24.83 mmHg (p<O.05), and plasma NO was reduced from 9.22?.28 i.tmol/l to 7.27-7.47 j.tmolll (p<O.05), no significant difference was found in plasma endothrlin-1. After 4h L-NAME infusion, values of mPAP and plasma NO come back to levels of untreated group but plasma endothrlin-1 got a significant increase (p(O.O5). It was suggested that the down-regulation of NO probably increased of pulmonary hypertension and ascites morbidity, and the up-regulation of NO probably inhibited the forming of pulmonary hypertension and reduced ascites morbidity.更多还原