Ehrlich H P, Grislis G, Hunt T K
Am J Surg. 1977 Jun;133(6):706-9. doi: 10.1016/0002-9610(77)90159-3.
Many theories have been proposed for the mechanism of wound contraction, that phenomenon of wound closure in which the skin surrounding the tissue defect is drawn into the open wound. When agents that inhibit microtubular function, such as vinblastine and colchicine, were topically applied to actively contracting wounds, contraction stopped. Cytochalasin B, an agent that reportedly disrupts microfilaments, did not alter contraction. These results suggest that wound contraction is related to the functioning of microtubules in fibroblasts within the wound and is proceeding at its maximal rate. The results tend not to support the theory that the microfilament components of cells are involved in wound contraction.
关于伤口收缩的机制已经提出了许多理论，伤口收缩是指组织缺损周围的皮肤被拉入开放性伤口的伤口闭合现象。当将抑制微管功能的药物，如长春碱和秋水仙碱，局部应用于正在积极收缩的伤口时，收缩停止。细胞松弛素B是一种据报道会破坏微丝的药物，它并没有改变收缩情况。这些结果表明，伤口收缩与伤口内成纤维细胞中微管的功能有关，并且正在以最大速率进行。这些结果倾向于不支持细胞的微丝成分参与伤口收缩的理论。
