Platelet activating factor antagonism in pure skin flaps exposed to ischaemia-reperfusion injury.
Platelet activating factor (PAF) is an inflammatory mediator that participates in neutrophil activation and adhesion to the endothelial cells. The PAF-antagonist (L-659.989) improves survival in myocutaneous flaps after ischaemia-reperfusion injury. To establish whether PAF antagonism improves survival in a pure skin flap, we subjected bilateral porcine buttock skin flaps (n = 14) to eight hours of ischaemia and 18 hours of reperfusion. L-659.989 or saline were given by local intra-arterial bolus infusion five minutes before reperfusion. There was no improvement in flap survival. Neutrophil accumulation as indicated by myeloperoxidase activity was increased in both groups compared with control tissue that had not been operated on (p < 0.01). There was no difference between treatment groups. Although it protected myocutaneous flaps, PAF antagonism did not protect pure skin flaps from ischaemia-reperfusion injury. A possible explanation is differences in flow-patterns that do not allow otherwise effective drugs to enter the area at risk, and so inhibit them from exerting a beneficial effect.
Birk-Sørensen
L
L
Microsurgical Research Laboratories, Royal Victoria Hospital, Montreal, Canada.
Kerrigan
C L
CL
Wang
C
C
D000818:Animals; D005260:Female; D005663:Furans / Q000494:pharmacology*; D018375:Neutrophil Activation; D009195:Peroxidase / Q000378:metabolism; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors*; D015427:Reperfusion Injury / Q000517:prevention & control*; D013524:Surgical Flaps / Q000098:blood supply; D013552:Swine
D005663:Furans; D010972:Platelet Activating Factor; C054893:L 659989; D009195:Peroxidase