一氧化氮对肉鸡肺动脉高压综合征的影响

肺动脉压升高是肉鸡肺动脉高压综合征(PHS)的重要发病机制。近年来研究表明一氧化氮(NO)在PHS发生发展中发挥着重要作用。本文论述了NO对肉鸡PHS发病过程的影响。一氧化氮合酶(NOS)和NO活性在PHS早期升高而后期下降。NO具有强大的扩张血管的作用,但在PHS过程中,NO合成相对不足,导致肺血管舒缩失衡,引起肺动脉压升高。肺血管重构是肉鸡肺动脉高压综合征的重要病理学变化特征,而NO可促进肺小动脉平滑肌细胞凋亡,在一定程度上抑制肺血管重构的形成。NO作为自由基对机体造成的损伤也是引起PHS的原因之一。在肉鸡日粮中补充NO前体物L-精氨酸可以增加内源性NO的生成,有助于降低PHS的发病率。

Effect of Nitric Oxide on PHS in Broiler

The mechanism for Pulmonary Hypertension Syndrome(PHS) in broiler is attributed to the increased pulmonary arterial pressure. More recently, it has been revealed that nitric oxide(NO) plays a vital role in PHS. This paper mostly reviewed the effect of NO on the development of PHS in broiler. It might be concluded that during the early period of the oxygen deficit spending, the activeness of nitric oxide synthase(NOS) elevates, thus causes the NO level elevate. But if the oxygen deficiting continuing,body can not react efficiently to alleviate this. The function of corresponding organ is damaged,further leading to PHS.NO is a potent vasodilator.However,the synthesize of NOS and NO is relatively insufficient during PHS.Consequentely, the unbalancedly stretch and constringency of the lung blood vessel results the pulmonary artery high pressure.Pulmonary vascular remodelling is one of the important pathological bases of PHS in broiler. NO has been found to induce apoptosis in pulmonary artery smooth muscle cells and to inhibit pulmonary vascular remodelling in broilers with pulmonary hypertension.In addition,NO can also cause PHS as one of the free radicals.Supplemental dietary L-arginine, the NO precursor,has been shown to increase the endogenous production of NO,reduce pulmonary arterial pressure,as well as the incidence of PHS in broilers.