The delay phenomenon: The story unfolds

Our previous studies have shown that when a flap is delayed, there is dilat ion of existing vessels within the flap not ingrowth of new vessels. The ma ximal anatomic effect on the arterial tree occurs at the level of the reduc ed caliber "choke" anastomotic vessels that link adjacent vascular territor ies. To further investigate the sequence of anatomic changes that occurs du ring the delay phenomenon, a large series of 200 rabbits and 17 dogs underw ent a flap delay procedure in either skin or muscle and the tissues were ex amined at postoperative periods between 1 hour and 1 year by using well-est ablished fluorescein, angiographic, light microscopic, immunohistochemical, and electron microscopic techniques. These data in the rabbit skin consistently demonstrated an initial period o f vasoconstriction that resolved within 3 hours postoperatively and was fol lowed by an active and progressive dilation of choke vessels that was most dramatic between 48 and 72 hours. In vivo intravenous fluorescein dye testi ng revealed an interesting parallel in that there was a temporary barrier t o the flow of fluorescein that occurred at the level of the choke vessels i mmediately after the flap was raised and that this temporary barrier contin ued to impede the flow toward the flap tip in rabbits where flaps had been delayed for periods up to 72 hours. Thereafter, there was Ilo obstruction t o the flow of fluorescein along the flap. During this early delay period of 3 days, light microscopy revealed a decrease ill vessel wall thickness ass ociated with an increase in lumen diameter. Over the next 4 days, the lumin al diameter continued to dilate to a lesser extent and the vessel wall thic kened. immunohistochemical analysis showed increased cell division, maximal between 24 and 72 hours, in all layers of the choke vessel wall. During th is same postoperative interval, transmission electron microscopy revealed p henotypic changes in smooth muscle cells from contractile to synthetic cell s. Hypertrophy of the smooth muscle cells was also observed. The vascular e ndothelium, which initially showed evidence of denudation, was restored to a healthy intact appearance within the first week after delay. When followed for longer periods, long-term studies of the delayed flap of up to 1 year demonstrated dramatically a permanent dilation of the choke ve ssel lumen and a thickening of the choke vessel wall. In canine studies, one rectus abdominis muscle was delayed by ligating the deep inferior epigastric artery. The time sequence of choke vessel dilation , studied by sequential angiograms in vivo, was comparable to that of the r abbit skin model. To ascertain the permanence and irreversibility of this d ilation, the normal circulation of the delayed rectus abdominis muscle was restored by reanastomosing the deep inferior epigastric artery. Even after a recovery period of up to 3 months, the choke vessels remained dilated and tortuous instead of reverting to their original narrow diameters. From this work, it is suggested that the choke vessel dilation seen in the delay period is a permanent and irreversible event. It is an active process associated with both an increase (hyperplasia) and an enlargement (hypertr ophy) of the cells in all layers of the choke artery wall and a resultant i ncrease in caliber of these vessels. The time sequence for delay appears to be similar in different species and in different tissues, suggesting the p ossibility of a universal process for delay.