Skin graft survival--the bacterial answer.
An in vitro wound model was created to determine the mechanism by which bacteria cause skin graft failure. A wound surface was simulated by a human fibrin clot. Staphylococcus aureus or group A streptococcus was incubated over the clot. Either saline, human plasminogen, aprotinin, or epsilon-aminocaproic acid (EACA), or a combination of these, was added to the tubes. After 30 hours, the tubes were examined for the presence of the clot. The supernatant was then examined for the presence of fibrin degradation products (FDP). S. aureus was incapable of destroying the fibrin clot without the presence of plasminogen in the culture media. Group A streptococcus was capable of some clot degradation, but this was markedly improved in the presence of plasminogen. High FDP levels correlated with the destruction of the clot. Both aprotinin and EACA were capable of preserving the fibrin clots. In this study we carefully controlled the chemical and bacterial milieu on a simulated wound.
Perry
A W
AW
Section of Plastic and Reconstructive Surgery, University of Chicago, IL.
Sutkin
H S
HS
Gottlieb
L J
LJ
Stadelmann
W K
WK
Krizek
T J
TJ
D000933:Antifibrinolytic Agents / Q000494:pharmacology; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006085:Graft Survival / Q000187:drug effects; D006801:Humans; D008954:Models, Biological; D010958:Plasminogen / Q000494:pharmacology; D012867:Skin / Q000382:microbiology; D016038:Skin Transplantation; D013211:Staphylococcus aureus / Q000502:physiology*; D013297:Streptococcus pyogenes / Q000502:physiology*
D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D010958:Plasminogen