Li G, Liang Y, Lu J
Department of Pathology, 304 Hospital of the PLA, Beijing 100037.
Zhonghua Bing Li Xue Za Zhi. 1998 Oct;27(5):337-40.
To study the role of nitric oxide (NO) in Hypoxic pulmonary hypertension (HPH).
NADPH-d and immunohistochemistry were used to study the expression and localization of constructive and inducible nitric oxide synthase (cNOS iNOS) in the lungs of normoxia and HPH rats, at the same time, the effects of L-arginine (L-arg) and nitro-L-arginine-methyl-ester (L-NAME) on normoxic and hypoxic pulmonary circulation were investigated.
NADPH-d positive expression was detected in the endothelium and smooth muscle cells (SMC) of large pulmonary vessels (PV) and in the epithelium and SMC of bronchi in the HPH group, but negative in the endothelium and SMC of small PV in normoxia. Hypoxia not only inhibited the expression of cNOS in the endothelium and SMC of PV and epithelium of bronchi, but also induced the expression of iNOS in the endothelium and SMC of PV and SMC of bronchi. Administration of L-NAME in normoxia had no effect on pulmonary circulation. The effect of administration of L-arg and L-NAME in hypoxia on right ventricular hypertrophy and remodeling of PV had no significance, compared with simple hypoxia.
The inhibition of cNOS may contribute to the occurrence of HPH, but induced iNOS may depress the development of HPH.
研究一氧化氮(NO)在低氧性肺动脉高压(HPH)中的作用。
采用还原型辅酶Ⅱ黄递酶(NADPH-d)组织化学和免疫组织化学方法,研究常氧及HPH大鼠肺组织中结构型和诱导型一氧化氮合酶(cNOS、iNOS)的表达及定位,同时观察L-精氨酸(L-arg)及硝基-L-精氨酸甲酯(L-NAME)对常氧和低氧肺循环的影响。
HPH组大鼠大肺动脉(PV)内皮细胞及平滑肌细胞(SMC)、支气管上皮细胞及SMC中均检测到NADPH-d阳性表达,而常氧组小PV内皮细胞及SMC中呈阴性。低氧不仅抑制PV内皮细胞及SMC、支气管上皮细胞中cNOS的表达,还诱导PV内皮细胞及SMC、支气管SMC中iNOS的表达。常氧下给予L-NAME对肺循环无影响。与单纯低氧相比,低氧时给予L-arg和L-NAME对右心室肥厚及PV重塑的影响无统计学意义。
cNOS的抑制可能参与HPH的发生,而诱导型iNOS可能抑制HPH的发展。