Briones Ana M, Salaices Mercedes, Vila Elisabet
Departament de Farmacologia, Terapèutica i Toxicología, Facultat de Medicina, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain.
J Gerontol A Biol Sci Med Sci. 2007 Jul;62(7):696-706. doi: 10.1093/gerona/62.7.696.
The mechanisms associated with structural and mechanical alterations of mesenteric resistance arteries from aged rats were investigated by using pressure myography, confocal microscopy, immunofluorescence, and picrosirius red staining. Arteries from old rats showed: (i) increased wall and media thickness, greater number of smooth muscle cell (SMC) layers but decreased density of SMC; (ii) increased number of adventitial cells; (iii) hypertrophy of nuclei of SMC and endothelial cells; (iv) increased stiffness associated with increased total collagen content and collagen I/III deposition in the media; and (v) similar content but changes in elastin structure in the internal elastic lamina. Hypertrophic outward remodeling in aged rat resistance arteries involve adventitial cells hyperplasia, reorganization of the same number of hypertrophied SMC in more SMC layers leading to thickened media and endothelial cell hypertrophy. Fibrosis associated with collagen deposition and changes in elastin structure might be responsible for the increased stiffness of resistance arteries from aged rats.
采用压力肌动描记法、共聚焦显微镜、免疫荧光和天狼星红染色法,研究了老年大鼠肠系膜阻力动脉结构和力学改变的相关机制。老年大鼠的动脉表现为:(i) 管壁和中膜厚度增加,平滑肌细胞(SMC)层数增多但密度降低;(ii) 外膜细胞数量增加;(iii) SMC和内皮细胞核肥大;(iv) 硬度增加,与中膜总胶原含量增加和I/III型胶原沉积有关;(v) 弹性蛋白含量相似,但内弹性膜弹性蛋白结构发生改变。老年大鼠阻力动脉的肥厚性向外重塑涉及外膜细胞增生、相同数量的肥大SMC在更多SMC层中重新排列,导致中膜增厚和内皮细胞肥大。与胶原沉积和弹性蛋白结构改变相关的纤维化可能是老年大鼠阻力动脉硬度增加的原因。