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The present study has been carried out in 10 dogs,in which fibronectinin wound fluid and plasma was measured with single radial immunodiffusion.Fibronectin in wound fluid rose from 24 h to 7 d after fracture.The meanincrease of fibronectin level was 0.79(P>0.01),1.76(P<0.01),3.07(P<0.001)and4.82(P<0.01)fold at 48,72 h,5 and 7 d,respectively,as comparison with 24 hafter fracture.Plasma fibronectin levels were markedly reduced 6 to 72 h afterfracture.The mean decline was 19.2％(P<0.01),18.0％(P<0.01),28.0％(P<0.01)and 9.2％(P<0.05)at 6,24,48 and 72 h,respectively.To our knowledge, therehas been no report on the regularity of the changes of fibronectin in wound fluidbefore,and a close correlation(r=0.9986;P<0.001) between the increase offibronectin levels and wound healing.A hypothesis,based on our study andcurrent literature,is presented that the increase of fibronectin in extracellularenvironment and the loss on cellular surface initiate,control and regulate themain biologic process of wound healing.
The present study has been carried out in 10 dogs, in which fibronectin in wound fluid and plasma was measured with single radial immunodiffusion. Fibronectin in wound fluid rose from 24 h to 7 d after fracture. The mean inflammation of fibronectin level was 0.79 (P> 0.01 ), 1.76 (P <0.01), 3.07 (P <0.001) and 4.82 (P <0.01) fold at 48, 72 h, 5 and 7 d, respectively, as compared with 24 hafter fracture. After 6 to 72 hours of treatment, the mean decline was 19.2% (P <0.01), 18.0% (P <0.01), 28.0% (P <0.01) and 9.2% , respectively.To our knowledge, therehas been no report on the regularity of the changes of fibronectin in wound fluid before, and a close correlation (r = 0.9986; P <0.001) between the increased offibronectin levels and wound healing. A hypothesis, based on our study and current literature, is presented that the increase of fibronectin in extracellularenvironment and the loss on the cellular surface, control and regulate the main biologic process of wound healing.