[链脲佐菌素致糖尿病大鼠皮肤创面初愈合过程的实验研究]。

Shika gakuho. Dental science reports Pub Date : 1989-04-01
A Nishigaki
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引用次数: 0

摘要

采用各种参数观察链脲佐菌素诱导糖尿病(STZ糖尿病)大鼠创面愈合过程。采用苏木精-伊红法、Van-Gieson法和Azan法染色切片,观察组织学变化。同时,测量愈合过程中创面强度作为评价愈合过程的参数。此外,测定白细胞、血浆纤维蛋白原、活化因子XIII (aXIII)、切口胶原含量及代谢变化。结果1。组织学研究表明,在STZ糖尿病中,炎症反应最小,发生时间比正常病例晚。在切开的伤口中,多形核白细胞的细胞浸润和纤维蛋白网积累不良。纤维蛋白网粗糙易碎。此外,伤口的上皮化较晚:直到手术后5天才发生。在STZ型糖尿病病例中,增生模式和成纤维细胞排列是异常的。胶原蛋白再生和增殖过程明显迟缓。2. 正常情况下,创面强度从术后第5天开始增加。10天后明显增高,30天后恢复到术前水平。而STZ型糖尿病患者术后14天内创面强度未见增加。此后,力量慢慢增强;但术后40天,仍未达到术前水平的80%。3.STZ型糖尿病患者白细胞的变化比正常人晚得多。恢复的时间比正常情况下要长。4. STZ型糖尿病患者血浆纤维蛋白原的升高和axii因子的降低较正常人慢。a - XIII因子明显降低,恢复缓慢。5. 在伤口切口胶原含量方面,STZ型糖尿病患者的胶原蛋白升高时间较正常人晚。但术后5 ~ 14天,其水平明显高于正常。成熟过程胶原蛋白和成熟胶原蛋白的增加速度更慢。正常情况下,术后20天成熟胶原已达到术前水平,而STZ糖尿病患者术后30天仍未达到80%的术前水平。6. 这些研究表明,以下因素阻碍了糖尿病患者的伤口愈合:炎症反应最小,纤维蛋白网不完全形成,上皮化迟缓,血浆纤维蛋白原和a - XIII因子的作用迟缓,成纤维细胞活性降低,胶原含量增加缓慢。
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[Experimental studies of skin wound healing process by first intention in streptozotocin-induced diabetes mellitus rats].

Various parameters were used in observing the process of wound healing in rats with streptozotocin-induced diabetes (STZ diabetes). Sections stained according to the Hematoxylin-Eosin, Van-Gieson, and Azan methods were used in observing histological changes. At the same time, wound strength during the healing was measured as a parameter for evaluating the healing process. In addition, changes in leukocytes, plasma fibrinogen, activated factor XIII (aXIII), collagen content of the incised wound, and metabolic changes were determined. Results 1. Histological studies showed that, in STZ diabetes, the inflammatory response was minimal and occurred later than in normal cases. In the incised wound, cellular infiltration of polymorpho-nuclear leukocytes and fibrin nets accumulated poorly. The fibrin net was coarse and fragile. Furthermore, epithelialization of the wound was late: it did not occur until 5 days after the operation. In cases of STZ diabetes, patterns of hyperplasia and fibroblast arrangements were abnormal. Collagen regeneration and proliferation processes were remarkably retarded. 2. In normal, wound strength increased from the 5 postoperative day. After 10 days had passed, it increased remarkably until, after 30 days, it had returned to the preoperative level. In STZ diabetes, however, no increase in wound strength occurred for the first 14 days after the operation. There after strength increased slowly; but, 40 days after the operation, 80% of the preoperative level still had not been reached. 3. Changes in leukocytes were much later occurring in STZ diabetes than in normal. Recovery took longer than in normal. 4. In STZ diabetes, increases in plasma fibrinogen and decreases of the aXIII factor were slower than in normal. The a XIII factor decreased remarkably, and recovery was slow. 5. In terms of collagen content in the wound incision, in STZ diabetes, tropocollagen increase occurred later than in normal. But, from the 5 to the 14 postoperative days, its level was higher than that in normal. Maturation-process collagen and mature collagen increased still more slowly. In normal, mature collagen had reached preoperative level 20 days after the operation, in STZ diabetes, 80% of preoperative level still had not been reached 30 days after the operation. 6. These studies showed that the following factors hinder wound healing in cases of diabetes mellitus: minimal inflammatory response, incomplete formation of the fibrin nets, retardation of epithelialization, retarded action of plasma fibrinogen and the a XIII factor, reduced fibroblast activity, and slow increase in collagen content.

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