Science

| Pre Clinical Studies |
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Shock waves were directed onto surgically compromised epigastric skin flaps in rats (Epos Fluoro, Dornier, 2500 pulses at 0.15 mJ/mm2). Flap viability of the eswt-treated rats were compared to those of also operated, but untreated animals. Necrotic zones in the eswt-treated flaps were significantly smaller (2.2% of the skin surface, versus 17.4%, p < 0.01) than in the untreated animals. Eswt seems to improve blood supply in ischemic tissue.
The effect of gene therapy with adenovirus-mediated TGF-beta or adenovirus mediated VEGF was compared to that of shock wave therapy on the rat, using the epigastric skin flap model (Epos Fluoro, Dornier, 2500 pulses at 0.15 mJ/mm2). Eswt enhances skin flap survival more than either Ad-TGF-beta treatment (eswt: 2.3% necrotic area, Ad-TGF-beta: 9.7 and control 17.4%, p < 0.05) or Ad-VEGF treatment (eswt: 2.23% necrotic area, Ad-VEGF: 9.25 and control: 17.4%, p < 0.05)
Ischemia was induced in transgenic mice by a tension-controlled hindlimb tourniquet. Ischemia was maintained for two hours, with subsequent reperfusion for 24 hours. Control animals received no treatment, whereas the animals of the shock wave group (Orthowave 180, MTS) received 50 percutaneous pulses on the ischaemic hindlimb 15 min prior to reperfusion. Increased perfusion levels (108%) were observed in the shock wave group. VEGF-R2 expression was significantly increased versus the control group after 4 hours.
In six horses a 4 cm diameter defect including skin, subcutis and periosteum was created on the metacarpi bilaterally. Esw was initiated on day 7 on one randomly selected metacarpus and repeated weekly until the wound was healed (EquiTron, SANUWAVE, 500 pulses at 0.11 mJ/mm2). The wound treated with esw healed in a mean of 76 days, as compared to 90 days for the untreated control (p=0.051).
A standardized epigastric skin flap model (left inferior epigastric vessel cut) was utilized to test whether the time point of esw application would influence the prevention of tissue necrosis. In the ischemic area 300 pulses at 0.1 mJ/mm2 (DermaGold, MTS) were applied at different time points: 24 h pre-OP, post-OP, 24 h post OP. In comparison to the control groups, all shock wave treated animals showed substantially reduced necrosis, regardless when they were esw treated. There was no difference within the shock wave groups.
A standardized epigastric skin flap model (left inferior epigastric vessel cut) was utilized in 16 rats to prove the effect of esw on the survival rate of the flap. Animals in the treatment group were exposed to 500 pulses at 0.15 mJ/mm on the entire right half of the flap (DermaGold, MTS, defocussed). Seven days after esw the necrotic area of the esw-treated animals was reduced by approx. 68%, compared to the control animals (11.7cm2 versus 3.8 cm2, p=0.0006). In a second experimental series, animals were euthanized after 12,24,48 and 72 hours in order to test for growth factors and stem cell marker analysis.
Thirty-six rats in a caudally based, random dorsal skin flap model were randomized into three groups: control group I without esw treatment, group II esw treated immediately post-op and group III immediately post-op plus one day following surgery (Ossatron, SANUWAVE, 500 pulses at 14 kV, equivalent to 0.15 mJ/mm2). Flap tissue blood perfusion was significantly increased three days post-operatively in group II (p < 0.005), and flap necrotic area in group II was significantly reduced seven days post-operatively compared with that of the control group (13±2.6% versus 42±5.7%, p < 0.01). There was only small and insignificant change in blood flow and necrotic area in group II compared with controls. Optimal dosage of esw treatment has a positive effect in rescuing ischemic skin flaps and is associated with suppressed topical tissue inflammation. Provided for educational purposes only; not to be copied or distributed without written consent. |
