MAINTENANCE OF QUALITY OF AGING BONE WITH ELECTRICITY

用电维持老化骨骼的质量

• 批准号: 3155596
• 负责人: Carl T. Brighton
• 金额: $ 14.12万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 1981
• 资助国家: 美国
• 起止时间: 1981-07-01 至 1988-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3155596
• 关键词: bone density; bone disuse atrophy; bone metabolism; calcium metabolism; cyclic AMP; denervation; disease /disorder prevention /control; eicosanoid metabolism; electrostimulus; fatty acid biosynthesis; indomethacin; mechanical stress; osteocytes; osteoporosis; pathologic bone resorption; proline; radiotracer; stimulus /response; thymidine; tibia; verapamil

It is the long-term objective of the proposed research to determine the electrical parameters required to prevent and reverse the loss of bone mass that occurs in osteoporosis. The sciatic neurectomized rat tibia will be continued to be used to complete the search for an optimal capacitively coupled electrical signal required to reverse an existing denervation disuse osteoporosis. The castrated rat vertebrae will be used as a hormone deficiency osteoporosis. In both osteoporosis models, various electrical signals will be evaluated as to their ability to reverse bone mass loss as determined by wet, dry, and ash weights and mechanical testing. The electrical field and current density induced in the rat tibia and vertebral body will be calculated such that the stage will be set to translate these findings into clinical application of the use of capacitive coupling in treating/preventing osteoporosis in the human. The proposed research will determine the dose-response characteristics of various capacitively coupled fields and various mechanical stresses on isolated bone cell 3H-thymidine, 35S, and 14C-proline incorporation, on cAMP and prostaglandin E2 synthesis, and on calcium flux into and out of the cell as determined by Quin-2, an intracellular calcium indicator. Indomethacin, a prostaglandin synthesis inhibitor, and verapamil, an agent which blocks membrane calcium channels dependent upon membrane depolarization, will be used to try to identify possible mechanisms of action of electrical and mechanical perturbations of isolated bone cells.

拟议研究的长期目标是确定 防止和逆转骨量损失所需的电参数 发生在骨质疏松症中。 坐骨神经切除的大鼠胫骨将 继续用于完成对最佳电容的搜索 逆转现有去神经支配所需的耦合电信号 废用骨质疏松。 被阉割的老鼠椎骨将被用作激素 缺乏性骨质疏松。 在两种骨质疏松症模型中，各种电 将评估信号逆转骨量损失的能力 通过湿重、干重、灰分重量以及机械测试来确定。 这 大鼠胫骨和椎骨中感应的电场和电流密度 身体将被计算，以便舞台将被设置来翻译这些 电容耦合在临床应用中的发现 治疗/预防人类骨质疏松症。 拟议的研究将确定剂量反应特征 各种电容耦合场和各种机械应力 分离的骨细胞 3H-胸苷、35S 和 14C-脯氨酸掺入， cAMP 和前列腺素 E2 的合成，以及钙离子流入和流出 由细胞内钙指示剂 Quin-2 测定的细胞。 吲哚美辛（前列腺素合成抑制剂）和维拉帕米（药物） 它阻断依赖于膜的膜钙通道 去极化，将用于尝试确定可能的机制 分离骨细胞的电和机械扰动的作用。