Kim S C, Seo K K, Kim I K, Kal W J, Lee M Y
Department of Urology, College of Medicine, Chung-Ang University, Seoul, Korea.
J Urol. 1999 Mar;161(3):964-9.
We evaluated effects of bacterial endotoxin during septicemia on contraction and relaxation responses of cavernous smooth muscles in rabbits.
We performed isometric tension studies with norepinephrine (NE), endothelium-dependent and endothelium-independent vasodilators, and nonadrenergic noncholinergic (NANC)-selective electrical field stimulation on the muscle strips of control and endotoxin (lipopolysaccharide; LPS)-treated rabbits. To determine reversibility of the LPS effects on the cavernous smooth muscle, the contraction and relaxation studies were repeated after resting the strips for 1 day at 4C. We also investigated the effect of the nonspecific nitric oxide synthase (NOS) inhibitor (NW-nitro-L-arginine methyl ester; L-NAME) and the selective immunologic NOS inhibitor (aminoguanidine) on reactivity of the strips to NE and acetylcholine.
Contractile response to NE was significantly (p <0.01) reduced in the cavernous smooth muscles from the systemically and locally LPS-treated rabbits, compared with control group. Both aminoguanidine and L-NAME markedly improved the diminished contraction of the strips. Relaxation response to endothelium-dependent agonists (acetylcholine and bradykinin) was significantly (p <0.05) decreased in the LPS-treated groups, compared with the control group but not to endothelium-independent vasodilators (papaverine and verapamil) and NANC-selective electrical field stimulation. L-NAME completely inhibited the relaxation response to acetylcholine in the control and LPS-treated groups but aminoguanidine did not. The impaired contraction and relaxation of the strips was completely restored after resting for 1 day.
Bacterial endotoxin may cause non-endothelial overproduction of NO and inhibition of endothelium-derived NO production, which may contribute to impairment of contraction and relaxation of rabbit cavernous smooth muscles.
我们评估了败血症期间细菌内毒素对兔海绵体平滑肌收缩和舒张反应的影响。
我们对对照组和内毒素(脂多糖;LPS)处理的兔的肌肉条进行了等长张力研究,使用去甲肾上腺素(NE)、内皮依赖性和非内皮依赖性血管舒张剂,以及非肾上腺素能非胆碱能(NANC)选择性电场刺激。为了确定LPS对海绵体平滑肌作用的可逆性,在4℃下将肌肉条静置1天后重复进行收缩和舒张研究。我们还研究了非特异性一氧化氮合酶(NOS)抑制剂(Nω-硝基-L-精氨酸甲酯;L-NAME)和选择性免疫性NOS抑制剂(氨基胍)对肌肉条对NE和乙酰胆碱反应性的影响。
与对照组相比,全身和局部LPS处理的兔的海绵体平滑肌对NE的收缩反应显著降低(p<0.01)。氨基胍和L-NAME均显著改善了肌肉条收缩减弱的情况。与对照组相比,LPS处理组对内皮依赖性激动剂(乙酰胆碱和缓激肽)的舒张反应显著降低(p<0.05),但对非内皮依赖性血管舒张剂(罂粟碱和维拉帕米)和NANC选择性电场刺激则无此现象。L-NAME完全抑制了对照组和LPS处理组对乙酰胆碱的舒张反应,但氨基胍没有。静置1天后,肌肉条受损的收缩和舒张完全恢复。
细菌内毒素可能导致非内皮源性一氧化氮过度产生并抑制内皮源性一氧化氮的产生,这可能导致兔海绵体平滑肌收缩和舒张功能受损。