As soon as the flap is elevated a complete disruption of blood flow takes place.
The functional loss of sympathetic innervation and the presence of ischemia compose a new status of hemodynamic imbalance for the isolated flap as flow decreases and vasoconstriction occurs by the release of sympathetic substances.
In order to survive the flap should restore an adequate nutritive process within the first 12 hrs postoperatively.
Initially, there is an increase in the size and the number of the small arteries of the subdermal plexus and of the dermal venous channels, plus a dilatation of preexisting anastomoses between transversely lying vessels 2' 4.
Tissue metabolism is switched to anaerobic as hypoxia occurs, resulting in decrease of oxygen, glycose and ATP and increase of lactate production, toxic superoxide radicals, prostacyclin, thromboxane and platelet aggregation.
The produced metabolic vasodilators enhance the flow and with the depletion of sympathetic vasoconstrictors there is a further increase from 12 - 48 hrs.
Angiogenetic "response" from the host tissue usually occurs 3-7 days after the transfer by direct in-growth and inoculation. Reorientation of vessels along the long axis and creation of functionally significant anastomosis take place in this period4.
Through the action of angiogenetic factors, a dilatation of the vessels at the edge of the flap occurs, basal membrane is thinned and there is migration of endothelial cells from the neighboring vascular lumen. Additionally, endothelial cells replicate in order to spread-out the new microvascular net and concomitantly anastomosing the capillaries forming loops and finally the new vascular "tree"4. Inoculation also occurs as some recipient capillaries are anastomosed with those of the flap 5.
After two weeks the circulation is well established between flap and recipient bed; the third week maturation of anastomoses continues and the third week flap achieves 90% of its final circulation4.
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