ABSTRACT
Objective To study the effect of dexamethasone to protect flaps from an ischemia-reperfusion injury and elucidate its mechanism of regulating the death course of the neutrophils. Methods The rats were randomly divided into 3 groups.The vein of the rat was clamped for 8 h after the flap had formed. Group A: the normal flap; Group B: the saline control flap; Group C: the treatment flap with dexamethasone. The survival area of the flaps was measured at 7 days; the apoptotic and necrotic neutrophils,tumor necrosis factor α (TNF-α), and interleukin 10 (IL-10) concentrations were measured. Results The flap survival are as in Groups A and C were larger than those in Group B. The apoptotic neutrophils in Group B were fewer than those in Groups A and C on the 1st and 3rd days after operation; however, they were more in number in Group B than in groups A and C on the 6th day. The necrotic cells in Group B were more in number than those in Groups A and C. In Group B, the plasma TNF-α concentration reached the maximum level at 1 h,while the IL-10 level reached the lowest 3 h after the reperfusion. In Group C, the TNF-α concentration was lower than that in Group B and decreased dramatically at 6 h. The IL-10 concentration was the lowest at 1 h, and increased rapidly at 3 h.Thus,ischemia-reperfusion could injure the flaps, probably through the abnormal action of the neutrophils, such as the disordered secretion of the cytokines and abnormal death course of the neutrophils. Conclusion Dexamethasone can protect the flap from an ischemia-reperfusion injury by its regulation for the neutrophil function.
ABSTRACT
Objective To study the role of sebaceous gland and its secretion in the progress of abnormal scar and to provide a new idea to prevent pathological scar. Method The sites, pathogenesis and pathological changes were compared between pathological and normal scars.Results Pathological scar often occurred at post-ear, upper lips, maxillofacial skin, and deltoid muscle skin of upper limbs; normal scar often occurred at mid-face, forehead, nose’s tip, and proximal extremity of limbs. Several rows of sebaceous gland and its secretion could be found at the edges of pathological scar, large quantity of sebaceous gland had changes of ductal dilation, and large amount of the secretion accumulated in the cavity in pathological scar; however, on the normal scar base and edges, seldomly showed the expanded sebaceous gland and accumulated secretion. Conclusions Sebaceous gland and its secretion could stimulate the growth of scar. To control the action of sebaceous gland and the formation of secretion could inhibit the formation of pathological scar.
ABSTRACT
Objective To investigate a better method for repair of scalp avulsion with skull exposure.Methods After primary debridement and skin grafting,tissue expanders were placed into subgaleal layer of normal scalp.After enough expansion,expanded scalp flaps were used to repair the skull exposure and the bald deformity.Results All of 6 cases had satisfactory results,wounds were repaired,no bald deformity occurred and no tissue expander infected case was encountered.Conclusion Using this method,we can treat the scalp avulsion with skull exposure without bald deformity.
ABSTRACT
Objective To find an effective method to prevent expanding flap from necrosis when expanders were removed. Methods After the expanders were removed, dexamethasone (5mg/kg) was injected into vein immeadiately when flaps showed blood flow disturbance, then decreased gradually and stopped until 6 days after operation. Results 33 of 35 patients recovered completely, and other 2 flaps survived mostly. Conclusion Dexamethasone given immeadiately could prevent expanding flap from necrosis.