Arthroscopic Subchondral Bone Plate Microfracture Technique Augments Healing of Large Chondral Defects in the Radial Carpal Bone and Medial Femoral Condyle of Horses

OBJECTIVE: To evaluate the effect of arthroscopic subchondral bone microfracture on healing of large chondral defects in horses. STUDY DESIGN: Short- (4 months) and long-term (12 months) in vivo experimental chondral defect model. ANIMALS: 10 horses, aged 2 to 5 years. METHODS: Each horse had a 1 cm2 full-thickness chondral defect created in both radial carpal bones and both medial femoral condyles. One carpus and one femoral condyle of each horse had the subchondral bone plate under the defect perforated using an orthopedic awl. All horses were exercised, five horses were evaluated after 4 months and five horses after 12 months. Gross, histologic, and histomorphometric examination of defect sites and repair tissues was performed, as was collagen typing of the repair tissue. RESULTS: On gross observation a greater volume of repair tissue filled treated defects (74%) compared with control defects (45%). Histomorphometry confirmed more repair tissue filling treated defects, but no difference in the relative amounts of different tissue types was observed. There was an increased percentage of type II collagen in treated defects compared with control defects and evidence of earlier bone remodeling as documented by changes in porosity. CONCLUSIONS: In full-thickness chondral defects in exercised horses, treatment with subchondral bone microfracture increased the tissue volume in the defects and the percentage of type II collagen in the tissue filling the defects when compared to nontreated defects. CLINICAL RELEVANCE: No negative effects of the microfracture technique were observed and some of the beneficial effects are the basis for recommending its use in patients cases with exposed subchondral bone.     

Effects of high and low inspired fractions of oxygen on horse erythrocyte membrane properties, blood viscosity and muscle oxygenation during anaesthesia

ObjectivesTo evaluate whether a period of hyperoxia or after a period of hypoxia produced changes attributable to reactive oxygen species in anaesthetized horses.Study designProspective randomized experimental study.AnimalsSix healthy (ASA I) geldings, aged 4.5–9.5 years and weighing 510–640 kg^?1.MethodsAfter 30 minutes breathing air as carrier gas for isoflurane, horses were assigned randomly to breathe air as carrier gas (CG0.21) or oxygen as carrier gas (CG1.00) for a further 90 minutes. After an interval of 1 month each horse was re-anaesthetized with the other carrier gas for the 90 minute test period. Ventilation was controlled throughout anaesthesia. Arterial blood was sampled to measure gas tensions, lactate, cholesterol, vitamin E, 4-hydroxy-alkenals, 8-epi-PGF_2α, half haemolysis time, half erythrolysis time, and erythrocyte membrane fluidity. Muscle blood flow and oxygenation were evaluated by near infrared spectroscopy and coloured Doppler.ResultsAfter the first 30 minutes horses were hypoxemic. Subsequently the CG1.00 group became hyperoxaemic (PaO₂～240 mmHg) whereas the CG0.21 group remained hypoxaemic (PaO₂～60 mmHg) and had increased lactate concentration. No significant changes in vitamin E, 4-hydroxy-alkenals, or 8-epi-PGF_2α concentrations were detected. During the 90 minute test period the CG0.21 group had increased resistance to free-radical-mediated lysis in erythrocytes, whereas the CG1.00 group had slightly decreased resistance of whole blood to haemolysis. CG0.21 induced a progressive muscle deoxygenation whereas CG1.00 induced an increase in muscle oxygen saturation followed by progressive deoxygenation towards baseline.Conclusions and clinical relevanceDuring isoflurane anaesthesia in horses, the hyperoxia induced by changing from air to oxygen induced minimal damage from reactive oxygen species. Using air as the carrier gas decreased skeletal muscle oxygenation compared with using oxygen.