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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.

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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). A second ischemic episode, such as thrombosis after free tissue transfer may be regarded as secondary (2 degrees) ischemia. The current study investigated 2 degrees ischemia in rodent epigastric flaps. Flaps were elevated in 50 Sprague-Dawley rats: group 1 had 5 hours 1 degree venous ischemia induced by placement of microvascular clamps; group 2 was like group 1, except venous continuity was re-established by venous anastomosis after resection of the venous segment previously microclamped; group 3 had 15 minutes of 1 degree ischemia, 24 hr later 5 hr of 2 degrees venous ischemia was induced by placement of microvascular clamps; group 4 was like group 3, except the venous segment was excised. Necrosis was evaluated on postoperative day 7. Both secondary ischemic groups had significantly less flap survival than the corresponding primary ischemic groups (P less than 0.001 for both). Resection of a portion of the vein and subsequent microanastomosis did not reduce flap survival (NS). Secondary venous ischemia of 5-hr duration is poorly tolerated by rodent skin flaps. There was no difference in flap survival in those flaps whose veins were clamped for 5 hr compared to those flaps whose clamped venous segments were resected and re-anastomosed.

Nitric oxide (NO) under basal conditions is an important regulator of vascular tone. Under ischemic conditions, however, NO can combine with superoxide anion to produce the damaging hydroxyl free radical. The current project observes the effect of inhibiting NO production (L-Nitro-amino-methyl-arginine, L-NAME) on flaps rendered ischemic by secondary (2 degrees) venous obstruction. Eighty rats had 3 x 6 cm skin flaps based on the epigastric vessels. Primary (1 degree) ischemia was produced by arteriovenous occlusion for 2 hours; (2 degrees) venous ischemia was induced by clamping the vein, alone for either 3 or 5 hours. Thirty minutes prior to 2 degrees ischemia, rats received either L-NAME (30 mg/kg) or saline buffer. Flap survival was assessed 7 days later and Chi-square analysis was used. At 3 hours of ischemia, treatment improved survival from 55% to 85% (P < 0.05). Treatment also improved survival at 5 hours of ischemia from 5% to 35% (P < 0.04). Although under resting conditions, NO is a potent vasodilator, during 2 degrees venous obstruction it may contribute to flap necrosis.