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ｐ＜０．０１同肺气肿相比，△ｐ＜０．０１，△△ｐ＜０．０１讨论ＣＰＨＤ早期心功能不全时，ＡＮＦ合成和释放增加，如心脏损伤进一步加重，心房内压明显升高，心房肌血供相对或绝对不足，最后导致心房内ＡＮＦ颗粒减少合成和释放障碍，甚至衰竭，有人发现随心衰程度加重，ＡＮＦ分泌逐渐减少。本研究显示：ＣＰＨＤ组与慢支组及肺气肿组相比，ＡＮＦ升高非常显著，而慢支组与肺气肿组之间相比升高不显著，机理为ＣＰＨＤ由于肾素血管紧张素醛固酮系统的激活，导致水钠潴留，循环血量增多，肺动脉压及右房压力增大，以而导致ＡＮＦ分泌增加，而慢支组及肺气肿组无肺动脉高压，因而升高不明显。ＥＴ主要是由内皮细胞分泌的人体中最强的缩血管物质。已有研究显示心衰越重，升高越明显，随心衰改善，就会下降，本研究进一步揭示，由慢支发展到肺气肿及ＣＰＨＤ，ＥＴ含量存在着显著差异，可能ＥＴ在此一病理过程中起着重要作用，由于ＥＴ收缩肺动脉及支气管动脉，将促进肺气肿与ＣＰＨＤ的发生发展，因而临床上寻找有效的ＥＴ抑制剂，对控制ＣＯＰＤ发展、改善ＣＰＨＤ患者生活质量有重大意义。
p <0.01 Compared with emphysema, △ p <0.01, △△ p <0.01 Discussion CPHD early cardiac insufficiency, ANF synthesis and release increased, such as further aggravating cardiac injury, intra-atrial pressure was significantly Elevated, atrial blood supply for relative or absolute lack of, and finally lead to atrial ANF particles to reduce the synthesis and release of obstacles, or even failure, it was found that with the severity of heart failure, ANF secretion decreased. This study showed: CPHD group compared with chronic bronchitis and emphysema group, ANF increased significantly, while chronic bronchitis group and emphysema group was not significantly increased compared to the mechanism of CPHD because of renin and vascular tension Activation of aldosterone system, leading to Shuinazhuliu, increased circulating blood volume, pulmonary pressure and right atrial pressure increased, resulting in increased ANF secretion, and chronic bronchitis and emphysema group without pulmonary hypertension, and thus increased significantly . ET is the strongest vasoconstrictor in the body secreted by endothelial cells. Studies have shown that more severe heart failure, the more obvious increase, improve with heart failure, will decline, further revealed that the development of chronic bronchi to emphysema and CPHD, ET content there is a significant difference, ET may be in this A pathological process plays an important role, because ET contraction of the pulmonary artery and bronchial artery, will promote the development of emphysema and CPHD, so the clinical search for effective ET inhibitors, to control the development of COPD, to improve the quality of life in patients with CPHD significant significance.