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首页> 外文期刊>American Journal of Physiology >Altered endothelium-dependent relaxations in lambs with high pulmonary blood flow and pulmonary hypertension.
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Altered endothelium-dependent relaxations in lambs with high pulmonary blood flow and pulmonary hypertension.

机译：高肺血流量和肺动脉高压的羔羊的内皮依赖性舒张改变。

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摘要

Congenital heart disease associated with increased pulmonary blood flow produces pulmonary hypertension. To characterize vascular alterations in the nitric oxide (NO)-cGMP cascade induced by increased pulmonary blood flow and pulmonary hypertension, 10 fetal lambs underwent in utero placement of an aortopulmonary vascular graft (shunt). When the lambs were 4-6 wk of age, we assessed responses of pulmonary arteries (PAs) and pulmonary veins (PVs) isolated from lungs of control and shunted lambs. PVs from control and shunted lambs relaxed similarly to exogenous NO (S-nitrosyl-acetyl-penicillamine), to NO produced endogenously (zaprinast and A-23187), and to cGMP (atrial natriuretic peptide). In contrast, relaxations to A-23187 and zaprinast were blunted in PAs isolated from shunted lambs relative to controls. Inhibitors of NO synthase (NOS) and soluble guanylate cyclase constricted control but not shunt PAs, indicating reduced basal NOS activity in shunt PAs. Pretreatment of shunt PAs with the substratesL-arginine and sepiapterin, a precursor for tetrahydrobiopterin synthesis, did not augment A-23187 relaxations. However, pretreatment with superoxide dismutase and catalase significantly enhanced A-23187 relaxations in shunt PAs. We conclude that increased pulmonary blood flow induces an impairment of endothelium-dependent relaxation that is selective to PAs. The impaired relaxation may be mediated in part by excess superoxide production.
机译：与肺血流量增加相关的先天性心脏病会产生肺动脉高压。为了表征由肺血流量增加和肺动脉高压引起的一氧化氮（NO）-cGMP级联中的血管改变，在子宫内放置了一个原肺血管移植物（分流器），对10只胎羊进行了研究。当羔羊的年龄为4-6周龄时，我们评估了从对照和分流羔羊的肺中分离出的肺动脉（PAs）和肺静脉（PVs）的反应。对照羔羊和分流羔羊的PVs类似于外源性NO（S-亚硝酰基-乙酰基-青霉胺），内源性产生的NO（zaprinast和A-23187）以及cGMP（心钠素）。相反，相对于对照，从分流羔羊中分离出的PA中，对A-23187和扎普林纳斯的松弛减弱。 NO合酶（NOS）和可溶性鸟苷酸环化酶的抑制剂限制了控制，但不限制分流PA，这表明分流PA的基础NOS活性降低。用底物L-精氨酸和Sepaapterin（四氢生物蝶呤合成的前体）预处理分流PA不会增加A-23187的弛豫。但是，用超氧化物歧化酶和过氧化氢酶预处理可显着增强并联PA中的A-23187松弛。我们得出结论，增加的肺血流量会引起对PAs选择性的内皮依赖性舒张功能的损害。松弛的减弱可能部分由过量的超氧化物产生介导。

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