Sites of inhaled NO-induced vasodilation during hypoxia and U-46619 infusion in isolated lamb lungs.
Sites of inhaled NO-induced vasodilation during hypoxia and U-46619 infusion in isolated lamb lungs.
复制标题
离体羔羊肺缺氧和输注 U-46619 期间吸入 NO 诱导的血管舒张部位。
DOI：
10.1152/ajpheart.1995.268.4.h1422
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Gordon,JB
中科院分区：
文献类型：
--
作者：
Tod,ML;O'Donnel,DC;Gordon,JB
在1 ~ 3月龄羔羊离体血液灌注肺中，用血管阻断技术研究了吸入一氧化氮（NO）引起的舒张部位。在一组10个肺，吸入NO（45 ppm）期间缺氧和U-46619诱导的肺血管收缩。在第二组5个肺中，比较了在U-46619诱导的高血压期间吸入NO和输注硝普钠（SNP，3微克·kg-1·min-1）的反应。缺氧引起显着的肺血管收缩，大小动脉和小静脉的压力梯度增加，定义为血管闭塞。吸入NO显著降低了67%的总肺动脉压差，并放松了大动脉和小动脉。输注U-46619导致所有节段压力梯度显著增加。吸入NO对大、小动脉和小静脉有舒张作用，但对大静脉无影响。输注SNP（一种被认为与内源性NO作用相似的亚硝基血管扩张剂）可引起与NO相似程度的总舒张（分别为81%和77%）。然而，与吸入NO相比，SNP可有效降低大肺静脉的压力梯度。这些结果表明，血红蛋白与吸入NO的快速结合并因此使其失活限制了其作为肺静脉扩张剂的功效。
The sites of relaxation in response to inhaled nitric oxide (NO) were investigated using the vascular occlusion technique in isolated blood-perfused lungs from 1- to 3-mo-old lambs. In one group of 10 lungs, inhaled NO (45 ppm) was administered during hypoxia- and U-46619-induced pulmonary vasoconstriction. In a second group of 5 lungs, responses to inhaled NO and infused sodium nitroprusside (SNP, 3 micrograms.kg-1.min-1) during U-46619-induced hypertension were compared. Hypoxia caused significant pulmonary vasoconstriction, with increases in the pressure gradients of large and small arteries and small veins, as defined by vascular occlusion. Inhaled NO significantly reduced the total pulmonary pressure gradient by 67% and relaxed both large and small arteries. Infusion of U-46619 caused significant increases in all segmental pressure gradients. While inhaled NO was effective in relaxing the large and small arteries and the small veins, it had no effect on the large veins. Infusions of SNP, a nitrosovasodilator thought to act like endogenous NO, caused a similar degree of total relaxation as NO (81 vs. 77%, respectively). However, in contrast to inhaled NO, SNP was effective in reducing the pressure gradient of the large pulmonary veins. These results suggest that rapid binding to and thus inactivation of inhaled NO by hemoglobin limit its efficacy as a pulmonary venous dilator.