Pulmonary vasodilation with structurally altered pulmonary vessels and pulmonary hypertension.
Pulmonary vasodilation with structurally altered pulmonary vessels and pulmonary hypertension.
复制标题
DOI：
10.1152/jappl.1988.65.6.2459
复制
发表时间：
1988-12
影响因子：
3.3
通讯作者：
E. Orton;J. Reeves;K. Stenmark
中科院分区：
文献类型：
--
作者：
E. Orton;J. Reeves;K. Stenmark
为了评估结构改变的肺血管床的肺血管舒张，我们在体内使用内皮依赖性（乙酰胆碱）和内皮非依赖性[硝普钠，前列腺素I2 (PGI2)]血管舒张剂，并分离患有严重肺动脉高压的新生小牛的大叶肺动脉。通过肺动脉输注乙酰胆碱，肺动脉压从120 +/- 7降至71 +/- 6mmhg，总肺阻力从29.4 +/- 2.6降至10.4 +/- 0.9 mmHg.l-1。不改变全身动脉压（90 +/- 5 mmHg）。虽然硝普钠和PGI2分别将肺动脉压降至86 +/- 4和96 +/- 4 mmHg，但它们也分别将全身动脉压降至65 +/- 4和74 +/- 3 mmHg。硝普钠和PGI2在降低总肺阻力（18.0 +/- 3.6和19.1 +/- 2.2 mmHg.l-1）方面都不如乙酰胆碱有效。分钟,分别)。乙酰胆碱可使经卵圆孔的右-左心脏分流从1.6 +/- 0.4 l/min降低至0.1 +/- 0.2 l/min，硝普钠和PGI2对右-左心脏分流无影响。来自肺动脉高压小牛的分离肺动脉在乙酰胆碱作用下没有松弛，而来自年龄匹配对照小牛的分离肺动脉在乙酰胆碱作用下有松弛。硝普钠对控制性肺动脉和肺动脉高压的影响同样良好。我们得出结论，乙酰胆碱在离体大叶肺动脉中的血管舒张功能在体外受到损害，但在体内对肺动脉高压新生儿的抵抗性肺动脉的血管舒张功能增强。
To evaluate pulmonary vasodilation in a structurally altered pulmonary vascular bed, we gave endothelium-dependent (acetylcholine) and endothelium-independent [sodium nitroprusside, prostaglandin I2 (PGI2)] vasodilators in vivo and to isolated lobar pulmonary arteries from neonatal calves with severe pulmonary hypertension. Acetylcholine, administered by pulmonary artery infusion, decreased pulmonary arterial pressure from 120 +/- 7 to 71 +/- 6 mmHg and total pulmonary resistance from 29.4 +/- 2.6 to 10.4 +/- 0.9 mmHg.l-1.min without changing systemic arterial pressure (90 +/- 5 mmHg). Although both sodium nitroprusside and PGI2 lowered pulmonary arterial pressure to 86 +/- 4 and 96 +/- 4 mmHg, respectively, they also decreased systemic arterial pressure to 65 +/- 4 and 74 +/- 3 mmHg, respectively. Neither sodium nitroprusside nor PGI2 was as effective as acetylcholine at lowering total pulmonary resistance (18.0 +/- 3.6 and 19.1 +/- 2.2 mmHg.l-1.min, respectively). Right-to-left cardiac shunt through the foramen ovale was decreased by acetylcholine from 1.6 +/- 0.4 to 0.1 +/- 0.2 l/min but was not changed by sodium nitroprusside or PGI2. Isolated lobar pulmonary arteries from pulmonary hypertensive calves did not relax in response to acetylcholine, whereas isolated pulmonary arteries from age-matched control calves did relax in response to acetylcholine. Control and pulmonary hypertensive lobar pulmonary arteries relaxed equally well in response to sodium nitroprusside. We concluded that acetylcholine vasodilation was impaired in vitro in isolated lobar pulmonary arteries but was enhanced in vivo in resistance pulmonary arteries in neonatal calves with pulmonary hypertension.