Abstract
Incised or excised wounds in the epidermis of Rhodnius nymphs or adults are healed by the following mechanisms: (i) "activation" or enlargement of the surrounding cells; (ii) migration of these epidermal cells and their crowding round the wound; (iii) a simultaneous accumulation of haematocytes; (iv) mitosis in the peripheral zone depleted of cells by this inward migration; (v) spreading of cells over the wound; (vi) the restoration of continuity in the epithelium, the secretion of new cuticle where needed and the degeneration of overcrowded or abnormal nuclei or nuclei that have come to lie outside the epidermis. In the healing of burns the migration of surrounding cells is much less marked and cell divisions occur chiefly among the cells spreading over the burned area. Evidence is given that migration of activated cells is a chemotactic response to the products of autolysis of proteins in the injured cells. Cells killed by heat are much less attractive. Proteins, especially hydrolysed proteins (peptones) from any source will stimulate this process. Dipeptide (glycyl-glycine) and free amino-acids have no effect. Glutathione and free cystein stimulate migration (perhaps by favouring autolysis). The occurrence of mitoses seems to be determined by sparseness among activated cells. Healing may occur without mitosis if the cells are sufficiently crowded, as in unfed nymphs. The healing reaction can be produced experimentally without interrupting the continuity of the epidermis. Thus destruction of continuity is not responsible for the initial reaction to injury; but the restoration of continuity appears necessary to bring about the cessation of new growth and the elimination of misplaced cells.

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