Flap necrosis occurs from a combination of reduced blood supply--a result of transection of the feeding vessels--and vasoconstriction. The vasoconstriction is secondary to the hyperadrenergic state that follows transection of the sympathetic nerves accompanying the vascular supply to the flap. A flap that has undergone surgical delay has had its stored neurotransmitter, norepinephrine, released and cleared from the tissues. At the time of the flap transfer, therefore, the hyperadrenergic condition does not reappear and the vascular flow is greater than in an undelayed flap.