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The purpose of this experimental study is to investigate the improvement in flap survival of prearterialization with delay procedure in venous flaps in rats. The transverse superficial inferior epigastric flap was utilized. Forty-six rats were randomized into four groups: group 1 as arterialized venous flaps, group 2 as venous flaps of prearterialization with delay procedure, group 3 as arterial perfusion venous flap, and group 4 as venous perfusion venous flap. Direct observation, histological analysis, and vascular perfusion examination by Indian ink injection were performed for flap assessment. The percentage of flap survival was 41.6 +/- 2.4%, 98.0 +/- 1.8%, 89.5 +/- 1.0%, and 11.3 +/- 0.8% in these four groups, respectively. Significant differences were noted between groups ( P < 0.05) except for between group 2 and group 3 ( P > 0.05). Vascular perfusion studies revealed that the Indian ink filled the entire flaps of group 2 in comparison with partially filled flaps in other groups. Histological examination showed more small vessels were observed through all layers of the flaps as well as dilated superficial veins in group 2 than those in other groups. In conclusion, prearterialization with delay procedure can improve the viability of the flap, and this method may be a strategy for flap prefabrication based on the venous network., (Copyright Thieme Medical Publishers.)

Dextran lowers the probability of thrombus formation, by reducing platelet aggregation and adhesion and by increasing fibrinolysis. All studies to date using dextran for microvascular reconstruction have examined only short-term (1 to 2 hr) patency in isolated vessels. The current study used an established thrombotic model (inverted sleeve interposition graft), to investigate the effect of dextran on the long-term survival of pedicle flaps. A6- x 3-cm epigastric flap was elevated. A 2-mm inverted sleeve interposition graft was placed on the artery side of the pedicle by microvascular techniques. One group received dextran (17 cc/kg) 2 hr preoperatively and every 6 hr postoperatively for the next 72 hr. A control group received saline on the same schedule. Survival was assessed on postoperative day 7, at which time necrosis was obvious. Several parameters (clotting studies and electron microscopy) were studied to characterize the phenomenon more clearly. Only 25 percent of saline-treated flaps survived (2/8), while all dextran-treated flaps survived (7/7) (p less than 0.02, Fisher exact test). Thus, dextran allowed flaps to survive by preventing thrombus formation, despite a strong thrombogenic focus.

In a previous study, timing relationships were studied for flaps subjected to secondary ischemia by total pedicle interruption. In the current paper, using a rodent epigastric flap, a similar study for flaps subjected to secondary ischemia by venous obstruction was performed. These conditions were designed to mimic a venous thrombosis following flap transfer, as would be performed clinically. In Experiment 1, the time interval between primary and secondary ischemia was varied. When the interval was 72 hr, flaps with secondary ischemia had similar survival to those with primary ischemia. However, when the time interval was 24 hr, flap survival after secondary ischemia was significantly worse than after primary ischemia (p less than 0.01). In Experiment 2, the duration of primary ischemia was varied (15 min, 30 min or 1.5 hr), prior to a fixed interval between primary and secondary ischemia and 5 hr of secondary ischemia. These conditions produced significantly more necrosis than 5 hr of primary ischemia. Thus, even short periods of primary ischemia may have detrimental effects on flap survival after a subsequent period of secondary ischemia. This may have important clinical ramifications.

The first ischemic insult a tissue suffers is primary (1 degree) ischemia. A second ischemic episode, such as thrombosis after free tissue transfer, may be regarded as secondary (2 degrees) ischemia. Timing relationships were studied in a rodent epigastric-flap model. In a first experiment, the interval between 1 degree ischemia and 2 degrees ischemia was varied. Flaps which had 2 degrees ischemia 12 and 36 hr after the 1 degree episode, had decreased ischemic tolerance, compared with 1 degree ischemic flaps; 2 degrees ischemic flaps, after an interval of 72 hr, had an ischemic tolerance similar to 1 degree ischemic flaps. In a second experiment, the length of the 1 degree ischemia was varied. It was found that as little as 5 min of 1 degree ischemia significantly decreased the subsequent tolerance of 2 degrees ischemia. The possible clinical significance of these results is discussed.

Arteriovenous flow reversal (AVR) has been used experimentally to salvage ischemic limbs and to create novel skin flaps with some success. The clinical applicability of AVR in muscle by way of two arteriovenous anastomoses in the rabbit was investigated. Twenty-four rabbits were divided into two groups. In Group 1 (control), the rectus femoris muscle was harvested and transplanted in the opposite thigh, anastomosing the donor femoral artery to the recipient femoral artery, and the donor rectus femoris vein to the recipient femoral vein. In Group 2 (flow reversal), the same procedure was done except the donor artery was anastomosed to the recipient vein and vice versa. Six and 24 hr postoperatively, specimens were compared macroscopically and by weight and histology. Reversed flow muscles were significantly heavier than control muscles at 6 hr and at 24 hr. Histologically, 6 hr of AVR caused edema, intramuscular hemorrhage, neutrophil infiltration, and thrombosis of most vessels. By 24 hr muscle cell degeneration was well advanced. All control muscles were viable, with only mild edema and slight peripheral necrosis. Possible reasons for the failure of AVR in muscle are discussed. On the basis of these results, AVR in free muscle transfer is not advocated.