Acceleration of dermal tissue repair by angiotensin II
Acceleration of dermal tissue repair by angiotensin II
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DOI：
10.1046/j.1524-475x.1997.50210.x
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发表时间：
1997-01-01
影响因子：
2.9
通讯作者：
Dizerega, Gere
中科院分区：
文献类型：
--
作者：
Rodgers, Kathleen;Abiko, Masami;Dizerega, Gere
血管紧张素 II 是一种天然存在的肽，已被证明具有血管生成特性，在此报告的研究中，血管紧张素 II 被证明可以以浓度依赖性方式增加培养的牛主动脉弓内皮细胞的增殖。在 Hydron 中急性施用血管紧张素 II 可加速全层切除大鼠模型中真皮损伤的修复。还进行了其他研究以确定将血管紧张素 II 递送至真皮损伤的最佳载体。几种载体，包括 10% 低粘度羧甲基纤维素、4% 中粘度羧甲基纤维素和 3% 高粘度羧甲基纤维素，被发现在这方面是有效的。确定损伤后第 0 至 4 天（第 0 天为手术时间）每日施用血管紧张素 II，以提供血管紧张素 II 加速伤口修复的最佳剂量。此外，剂量反应研究表明，血管紧张素II以剂量依赖性方式加速伤口修复，第0至4天施用的血管紧张素II分别为0.03和0.01μg/大鼠/天，分别是最低有效剂量和无效剂量。还发现，在愈合受损的动物（类固醇和阿霉素治疗的大鼠和糖尿病小鼠）受伤后，每天给予 100 μg 血管紧张素 II 10% 羧甲基纤维素溶液 5 天，可以加速修复速度。总之，在正常和受损动物模型中，血管紧张素 II 以剂量依赖性方式加速全层皮肤损伤的闭合。
Angiotensin II is a naturally occurring peptide which has been shown to possess angiogenic properties, in the studies reported here, angiotensin II was shown to increase the proliferation of cultured bovine aortic arch endothelial cells in a concentration-dependent manner. Acute administration of angiotensin II in Hydron accelerated the repair of dermal injuries in a full-thickness excisional rat model. Additional studies were done to determine the best vehicle for delivery of angiotensin II to a dermal injury. Several vehicles, including 10% low-viscosity carboxymethyl cellulose, 4% medium-viscosity carboxymethyl cellulose, and 3% high-viscosity carboxymethyl cellulose, were found to be effective in this regard. Daily administration of angiotensin II for days 0 to 4 after injury (day 0 being the time of surgery) was determined to provide the optimal dosage for acceleration of wound repair by angiotensin II. In addition, dose-response studies indicated that angiotensin II accelerated wound repair in a dose-dependent fashion with 0.03 and 0.01 mu-g/rat/day of angiotensin II administered on days 0 to 4 being the minimally effective and no-effect doses, respectively. Administration of 100 mu-g/day of angiotensin II in 10% carboxymethyl cellulose for 5 days after injury to animals with impaired healing (steroid- and adriamycin-treated rats and diabetic mice) was also found to accelerate the rate of repair. In conclusion, angiotensin II accelerated the closure of full-thickness skin injuries In a dose-dependent manner in normal and impaired animal models.