[Modulation of the neutrophil died process-mechanisms of the flap protection from ischemia-reperfusion with dexamethasone].

OBJECTIVE: To study the modulation of neutrophil apoptosis and necrosis, elucidate the protecton mechanisms of dexamethasone. METHODS: 50 rats were divided into 5 groups. I: normal island flap. II: artery occlusion for 8 hours, saline given into peritoneal. III: venous occlusion for 8 hours, saline given into peritoneal. IV: artery occlusion for 8 hours, dexamethasone injected through peritoneal. V: venous occlusion for 8 hours, dexamethasone injected through peritoneal. Flap survived areas were measured, neutrophil apoptosis and necrosis values were ananlyzed with FCM. Their morphology were observed with light microscopy. The swallows of apoptotic neutrophil by mascrophages were studied with transmission electron microscopy. RESULTS: Flap survived areas I, IV and V groups were higher than that in II and III groups, which in I, IV, V had no significant values. Apoptotic neutrophils values in II and III groups on 1, 3 days were less than that in, but on 6 days, higher than that in I, IV and V. Necrotic neutrophils showed another tendency postoperatively when compared with its apoptotic values. There were more swallows of apoptotic neutrophils in flaps of IV, V groups than that in II, III flaps. CONCLUSION: Dexamethasone's flap protection results from modulating of neutrophils apoptosis, decreasing it's necrosis, increasing swallowings values of apoptotic neutrophils by macrophages.

[Systemic influence after an island flap with venous congestion-reperfusion injury].

OBJECTIVE: To investigate the systemic influence after an island flap with venous congestion-reperfusion. METHODS: An island flap was formed in a Rat model. The vein in the pedicle was clamped for 2 hours, 6 hours and 10 hours and released. The ear microcirculation, levels of TNF alpha and IL-10 were measured, and the neutrophils sequestration in tissues were counted. The vascular structure of the lung and intestine were evaluated. RESULTS: There were significant changes in the ear microcirculation, neutrophils sequestration of the lung and the intestine in the 2 hours, 6 hours and 10 hours groups, and became more serious by the time increasing. The TNF alpha level reached in maximum at 1 hour after the reperfusion, while the IL-10 became to the lowest level at 3 hours after the reperfusion. However, the TNF alpha and IL-10 levels were significant high in the 6 hour and 10 hours groups, compared with the 2 hours group and the control, but there was no differences between the2 hours group and the control. CONCLUSIONS: Venous congestion-reperfusion of flap could injury the remote organs such as lung, intestinal etc. The injury could be more serious with the time increasing.

[A clinical study of flap necrosis protection with dexamethasone].

OBJECTIVE: This clinical study was to find an effective method to prevent flap from necrosis. METHODS: When a flap showed blood flow problems, dexamethasone of 0.3 mg/kg was given intravenously for 2 days. Then the dose was decreased to 0.2 mg/kg at the third and the fourth day. At the fifth and the sixth day, dexamethasone of 0.1 mg/kg was given. RESULTS: A total of 51 flaps with blood flow problems was treated with this method. Thirty of them recovered completely; 18 survived mostly and 3 failed. CONCLUSION: Early application of dexamethasone can effectively ameliorate blood flow problems of the flap.

[Hemorheology of island flap after ischemia-reperfusion injury and modulation of dexamethasone].

OBJECTIVE: To study the hemorheology of island flap after ischemia-reperfusion injury and modulation of dexamethasone. METHODS: Sixty Wister rats were made ischemia-reperfusion injury model, and divided into two groups randomly(Group I: intraperitoneal injection of normal saline 2 ml/kg as control group; Group II: intraperitoneal injection of dexamethasone 5 mg/kg as experimental group). Flap survived areas were measured and neutrophil necrosis numbers in flaps were counted. Erythrocytes and neutrophil hemorheology were observed. RESULTS: Area survived flap in group II was larger than that in group I. Neutrophil necrosis numbers were less in group II than in group I (P < 0.05). Whole blood hyposhear viscosity, erythrocyte aggregation, Casson yield stress and nerutrophil adhesion ability were higher in group I than in group II (P < 0.05); and the neutrophil deformability was lower in group I than in group II. CONCLUSION: Flap inchemia-reperfusion can increase erythrocyte aggregation index and neutrophil adhesion ability. Dexamethasone can improve these and decrease neutrophil necrosis numbers, so as to prevent flap from ischemia-reperfusion injury.