Ogawa T, Morioka Y, Inoue T, Takano M, Tsuda S
Pharma Research and Development Division, Hoechst Japan Ltd., Saitama-ken.
Inflamm Res. 1995 Jun;44(6):264-8. doi: 10.1007/BF01782980.
An involvement of blood coagulation factor XIII (FXIII) in healing of burns was examined in rats with the carbon tetrachloride (CCl4)-induced hepatic injury. The oral administration of 2 and 4 ml/kg CCl4 to rats every 4 days delayed healing of the burns induced on the back skin and decreased FXIII activity. These animals showed some hepatotoxic signs (increased glutamic-oxaloacetic and glutamic-pyruvic transaminases) and accelerated blood coagulation system (increased fibrino-peptide A and fibrin degradation product). The delay in the burn healing was shortened by repeated intravenous injections with normal human placenta-derived FXIII concentrate (Fibrogammin P; 120 U/body) every 4 days. There was a negative correlation between plasma FXIII activity at the end of experiment and the time required for wound healing. These findings suggest that reduction in FXIII activity may be one of the factors inducing delayed wound healing in the CCl4-induced hepatic injury rats.
在四氯化碳（CCl4）诱导肝损伤的大鼠中，研究了凝血因子XIII（FXIII）在烧伤愈合中的作用。每4天给大鼠口服2和4 ml/kg CCl4会延迟背部皮肤烧伤的愈合，并降低FXIII活性。这些动物出现了一些肝毒性体征（谷氨酸草酰乙酸转氨酶和谷氨酸丙酮酸转氨酶升高）以及加速的凝血系统（纤维蛋白肽A和纤维蛋白降解产物增加）。每4天重复静脉注射正常人胎盘来源的FXIII浓缩物（纤维蛋白原；120 U/只）可缩短烧伤愈合延迟时间。实验结束时血浆FXIII活性与伤口愈合所需时间呈负相关。这些发现表明，FXIII活性降低可能是CCl4诱导肝损伤大鼠伤口愈合延迟的因素之一。
