Reconstruction of orbicularis oris and levator labii superioris muscles in secondary repair of unilateral cleft lip.

We devised a new method to repair the depression of the nasal floor and inferolateral displacement of the alar base and to reconstruct the philtrum in the secondary repair of unilateral cleft lip. Depression of the nasal floor and inferolateral displacement of the alar base were corrected by advancing a lump of the levator labii superioris, the levator labii superioris alaeque nasi, and the upper part of the superficial orbicularis oris muscles to the anterior nasal spine. When the depression of the nasal floor was too severe to repair using these muscles only, a cranially-based de-epithelialised flap of the scar region on the upper lip was inserted under the nasal floor. The lower, greater part of the superficial orbicularis oris muscle was dissected to the nasolabial fold, brought towards the midline, and laid on the surface of the same muscle on the medial side to be sutured. When the depression of the nasal floor was not severe, the lower, greater part of the superficial orbicularis oris muscle was passed through a tunnel pierced beneath the de-epithelialised scar tissue and sutured to the corresponding components on the medial side to reinforce the philtral ridge. In both cases, if the deep orbicularis oris muscle in the vermilion had been interrupted, it was reconstructed by end-to-end anastomosis. Operative results were evaluated in 76 patients using photographs taken preoperatively and postoperatively. Elevation of the nasal floor and correction of the alar base were achieved in most patients, while reconstruction of the philtrum was achieved in cases in which the skin tension at the suture line was weak.

Formation of 4-hydroxy-2-nonenal-modified proteins and 3-nitro-L-tyrosine in rat island skin flaps during and after ischemia.

4-Hydroxy-2-nonenal (HNE)-modified proteins and 3-nitro-L-tyrosine were evaluated as a specific marker of reactive oxygen species (ROS)- and nitric oxide (NO)-mediated peroxynitrite-induced tissue injuries in ischemic and reperfused skin flap by Western blot analysis. Specimens were taken from island skin flaps of rats during the following three conditions: ischemia only, 5 hours of ischemia and reperfusion, and 10 hours of ischemia and reperfusion. HNE-modified proteins and 3-nitro-L-tyrosine increased with ischemic time (3, 6, and 10 hours postischemia). In the reperfused skin flap after both 5 and 10 hours of ischemia, HNE-modified proteins and 3-nitro-L-tyrosine were increased 3 hours postreperfusion, and they reached a maximum 6 hours after reperfusion. HNE-modified proteins and 3-nitro-L-tyrosine 1 hour postreperfusion were higher with 10 hours ischemia-reperfusion than with 5 hours ischemia-reperfusion. These results indicate (1) that ROS- and NO-induced peroxynitrite-mediated cytotoxicity in ischemic flaps is dependent on the ischemic period and (2) that ROS- and NO-induced peroxynitrite-mediated cytotoxicity occurs during an early stage of reperfusion if the ischemic period is long.

Cellular artificial skin substitute produced by short period simultaneous culture of fibroblasts and keratinocytes.

We developed a novel artificial skin substitute consisting of two collagen sponge layers with different pore sizes and cross-link densities. Fibroblasts suspended in 0.5 ml Dulbecco-modified Eagle's medium (DMEM) + 10% fetal bovine serum (FBS) were seeded on the lower dermal sponge layer, then epidermal collagen sponge and 0.1 ml suspension of keratinocytes in KGM were layered in this order. After a few hours, the medium was changed to DMEM + 5% FBS. These processes were carried out in one day, and the composite layers were then cultured by the air-liquid interface culture method. Three to five days after seeding, keratinocytes had grown to about ten layers, and fibroblasts had grown three-dimensionally into the lower dermal sponge layer. This novel cellular artificial skin substitute was grafted onto nude mice and took in 4 weeks. This skin substitute has the advantage of a shorter culturing period than previously cultured skins, and may be clinically useful for grafting that is urgently required in patients with severe generalised burns.

Versatility of modified planimetric Z-plasties in the treatment of scar with contracture.

The planimetric Z-plasty proposed by Roggendorf provides elongation by excision of a pair of triangular pieces of tissue. The application of planimetric Z-plasties has been modified by making the vertical angle flexible, and making them continuous in the same or in opposite directions. Continuous planimetric Z-plasties in the same direction elongate an oblique contracture in the longitudinal direction. Continuous planimetric Z-plasties in an alternative direction elongate a disproportioned scar contracture in the longitudinal direction. Both techniques partially reduce unsightly scarring. Furthermore, they can be used in combination with V-Y-plasties. These modifications permit rational planing of the treatment of complicated scars with contracture.

Involvement of nitric oxide in survival of random pattern skin flap.

A free radical gas, nitric oxide, has many useful functions when produced under physiological conditions by neurons and endothelial cells. However, excess nitric oxide has been reported to exert cytotoxic effects by direct toxicity or by reaction with superoxide. The effect of nitric oxide on the microcirculation in the periphery of a flap remains unclear, and its effect on flap survival is also unknown because nitric oxide has a dual action. Thus, we attempted to clarify the effect of nitric oxide on survival of rat random pattern skin flaps by the use of an endothelial constitutive nitric oxide synthase inhibitor (i.p. administration of 50 mg/kg N(G)-nitro-L-arginine) and the substrate of nitric oxide synthase (i.p. administration of 1 g/kg L-arginine). Three kinds of experiments were done using a total number of 120 animals: (1) time course measurement of blood flow in the flap periphery was performed using a laser Doppler flowmeter (30 rats), (2) the length of the surviving area of flaps was measured 1 week after raising the flap (60 rats), and (3) Western blot analysis was used to determine the time course of changes in the amount of endothelial constitutive nitric oxide synthase and the formation of 3-nitro-L-tyrosine, which is a marker of peroxynitrite-mediated (i.e., nitric oxide-dependent) tissue damage (30 rats). Inhibition of endothelial constitutive nitric oxide synthase by N(G)-nitro-L-arginine significantly decreased the length of the surviving area of skin flap (p < 0.01 compared with the control), which was associated with a decrease in the blood flow of the proximal portion of the flap. On the other hand, exogenous L-arginine increased the survival length of skin flap significantly (p < 0.01 compared with the control), which was associated with an increase in blood flow of the distal portion of the flap even though there was nitric oxide-mediated oxidative tissue damage. These results suggest that nitric oxide produced by endothelial constitutive nitric oxide synthase plays a role in maintaining circulation in the skin flap periphery and that L-arginine administration contributes to reduction of ischemic necrosis in the skin flap.