Martínez C, Cases E, Vila J M, Aldasoro M, Medina P, Marco V, Lluch S
Departamento de Fisiología, Universidad de Valencia, Spain.
Eur Respir J. 1995 Aug;8(8):1328-32. doi: 10.1183/09031936.95.08081328.
The present study was designed to investigate the contribution of the endothelium and that of the L-arginine pathway on the contractile responses of isolated human pulmonary arteries to electrical field stimulation (EFS) and noradrenaline. Isometric tension was measured in artery rings obtained from portions of human lung after thoracic surgery for removal of lung carcinoma (18 patients). Electrical field stimulation (EFS) induced frequency-dependent contractions of isolated human pulmonary arteries which were abolished by tetrodotoxin, guanethidine and prazosin (all at 10(-6) M). The increases in tension were of greater magnitude in arteries denuded of endothelium. NG-nitro-L-arginine methyl ester (L-NAME) (10(-4) M) potentiated the contractile response to EFS in artery rings with endothelium but not in endothelium-denuded arteries. The potentiation induced by L-NAME was completely reversed by L-arginine (10(-4) M) but not by D-arginine (10(-4) M). Indomethacin (3 x 10(-6) M) had no significant effect on the contractile response to EFS. Contractile responses to noradrenaline were similar in arteries with and without endothelium. Our results suggest that electrical field stimulation releases endothelium-derived nitric oxide, which inhibits the contractile responses of human pulmonary arteries. Although adrenergic nerves seem to be responsible for the contraction, the transmitter involved in the release of nitric oxide does not appear to be noradrenaline.
本研究旨在探讨内皮和L-精氨酸途径对离体人肺动脉对电场刺激（EFS）和去甲肾上腺素收缩反应的作用。在因肺癌行胸外科手术切除肺组织的患者（18例）所取的动脉环中测量等长张力。电场刺激（EFS）可引起离体人肺动脉频率依赖性收缩，这种收缩可被河豚毒素、胍乙啶和哌唑嗪（均为10⁻⁶ M）阻断。内皮剥脱的动脉中张力增加幅度更大。NG-硝基-L-精氨酸甲酯（L-NAME）（10⁻⁴ M）增强有内皮动脉环对EFS的收缩反应，但对内皮剥脱的动脉无此作用。L-NAME诱导的增强作用可被L-精氨酸（10⁻⁴ M）完全逆转，但不能被D-精氨酸（10⁻⁴ M）逆转。吲哚美辛（3×10⁻⁶ M）对EFS的收缩反应无显著影响。有内皮和无内皮的动脉对去甲肾上腺素的收缩反应相似。我们的结果表明，电场刺激释放内皮源性一氧化氮，其抑制人肺动脉的收缩反应。虽然肾上腺素能神经似乎是收缩的原因，但参与一氧化氮释放的递质似乎不是去甲肾上腺素。
