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交感神经切除术会改变成年生长中大鼠的骨骼结构。

Sympathectomy alters bone architecture in adult growing rats.

作者信息

Pagani F, Sibilia V, Cavani F, Ferretti M, Bertoni L, Palumbo C, Lattuada N, De Luca E, Rubinacci A, Guidobono F

机构信息

Department of Pharmacology, Chemotherapy and Medical Toxicology, University of Milan, Milan, Italy.

出版信息

J Cell Biochem. 2008 Aug 15;104(6):2155-64. doi: 10.1002/jcb.21775.

Abstract

Sympathetic nervous system (SNS) fibres and alpha- and beta-receptors are present in bone, indicating that the SNS may participate in bone metabolism. The importance of these observations is controversial because stimulation or inhibition of the SNS has had various effects upon both anabolic and catabolic activity in this tissue. In this study we evaluated the effects of pharmacological sympathectomy, using chronic treatment of maturing male rats with 40 mg of guanethidine/kg i.p., upon various parameters in bone. Double labelling with tetracycline injection was also performed 20 and 2 days before sacrifice. Bone mass, mineral content, density and histomorphometric characteristics in different skeletal regions were determined. Bone metabolic markers included urinary deoxypyridinoline and serum osteocalcin measurements. Guanethidine significantly reduced the accretion of lumbar vertebral bone and of mineral content and density, compared to controls. Femoral bone mineral content and density were also significantly reduced, compared to controls. Histomorphometric analyses indicated these effects were related to a reduction of cortical bone and mineral apposition rate at femoral diaphysials level. Both markers of bone metabolism were reduced in controls as they approached maturity. Guanethidine significantly decreased serum osteocalcin compared to controls, while urinary deoxypyridinoline was unchanged. These data indicate that guanethidine-induced sympathectomy caused a negative balance of bone metabolism, leading to decreased mass by regulating deposition rather than resorption during modeling and remodeling of bone.

摘要

交感神经系统(SNS)纤维以及α和β受体存在于骨骼中,这表明交感神经系统可能参与骨代谢。这些观察结果的重要性存在争议,因为刺激或抑制交感神经系统对该组织的合成代谢和分解代谢活动都产生了各种影响。在本研究中,我们评估了药物性交感神经切除术的效果,即对成熟雄性大鼠腹腔注射40mg胍乙啶/kg进行长期治疗,观察其对骨骼各项参数的影响。在处死前20天和2天还进行了四环素注射双重标记。测定了不同骨骼区域的骨量、矿物质含量、密度和组织形态计量学特征。骨代谢标志物包括尿脱氧吡啶啉和血清骨钙素的测量。与对照组相比,胍乙啶显著降低了腰椎骨的增生以及矿物质含量和密度。与对照组相比,股骨的矿物质含量和密度也显著降低。组织形态计量学分析表明,这些影响与股骨骨干水平皮质骨的减少和矿物质沉积率的降低有关。随着对照组接近成熟,两种骨代谢标志物均降低。与对照组相比,胍乙啶显著降低了血清骨钙素,而尿脱氧吡啶啉未发生变化。这些数据表明,胍乙啶诱导的交感神经切除术导致骨代谢负平衡,在骨骼建模和重塑过程中通过调节沉积而非吸收导致骨量减少。

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