急、慢性缺氧对肺组织一氧化氮合成酶活性的影响

被引：13

作者：

袁予辉

王迪浔

机构：

[1] 同济医科大学病理生理教研室!武汉,,同济医科大学病理生理教研室!武汉,

来源：

中国病理生理杂志 | 1997年 / 06期

关键词：

一氧化氮; 酶类; 血缺氧; 肺动脉;

D O I：

暂无

中图分类号：

R363 [病理生理学];

学科分类号：

100104 ;

摘要：

本文利用β－NADPH－d组织化学法发现，急性缺氧时肺动脉内皮之一氧化氮合成酶（nitricoxidesynthase,NOS）阳性着色降低，而肺组织中NOS阳性神经纤维数目增多及着色明显增强，呈典型串珠状，并可见神经元及丝状神经纤维。同时见支气管上皮的Nos着色略降低。慢性缺氧时，肺动脉内皮增厚、充盈，NOS着色加深，而支气管上皮NOS着色更加降低。因此，急性缺氧所致肺动脉收缩反应可能与内皮NO生成减少有关，但通过NOS阳性神经纤维兴奋，释放NO对HPV起调节作用。慢性缺氧时内皮NOS活性及含量升高，对肺动脉高压的形成起调节作用。

引用

页码：566 / 569

页数：4

共 7 条

[1]

Repeated endothelial removal augments inimalthickening and attenuates EDRF release. Yasunari N. American Journal of Physiology . 1994

[2]

Structural changes reduced endothelium-dependent relaxation in chronic obstructive lung dis-ease. Din-Xuan AT. The New England Journal of Medicine . 1991

[3]

Hypoxia inhibits expression ofeNOS via beription and posttranscription mechanisms. MmQullan LP,Gordon KL. American Journal of Physiology . 1994

[4]

Methylene blue potentiatesvascular reactivity in isolated rat lungs. Mazmanian GM,Baudet B. Journal of Applied Physiology . 1989

[5]

Increased endothlium-derivedNO in hypertensive pulmonary cireulation of chronicallyhypokic rats. Isaacson TC,Hampl V. Journal of Applied Physiology . 1994

[6]

Nitric oxide synthase and neuronal β-NADPH diaphorase are identical inbrain and peripheral tissues. Dawson TM,Bredt DS,Fotuhi M,et al. Proceedings of the National Academy of Sciences of the United States of America . 1991

[7]

Endothelium-derived edaxing factoridhibits hypoxic pulmonary vaseonstrichon in rats. liu SF,Crawley DE. The American Review of Respiratory Disease . 1991

← 1 →