Vascularization of Split-Thickness Skin Autografts in the Rat

Histochemical studies of diphosphopyridine nucleotide diaphorase activity, using neotetrazolium salts as reagents, were undertaken in split-thickness skin autografts in rats, removed with a dermatome, and replaced on the donor dermal bed. In contrast to an early and rapid loss of diaphorase activity in the pre-existing blood vessels of full-thickness grafts placed on a suprapannicular bed, the delayed and slower decline of activity in such vessels in the split-thickness grafts suggests that the onset and rate of degenerative changes in these vessels vary with the thickness of the graft; in thin grafts nutrient fluids during the phase of plasmatic circulation have a shorter distance to travel and the thin graft has fewer cellular elements requiring nourishment. Histochemical and stereomicroscopic studies of the split-thickness grafts show that the vascular ingrowth originates from the distended blood vessels lying in the deep host dermal layer immediately superjacent to the panniculus carnosus, not from the vessels at the surface of the host dermal bed in contact with the graft. The revascularization of the split-thickness graft on a dermal host bed occurs at the same rate as that of a full-thickness graft on a suprapannicular bed.