Effects of plasma rich in growth factors (PRGF) on biomechanical properties of Achilles tendon repair.

PURPOSE: To assess the biomechanical effects of intra-tendinous injections of PRGF on the healing Achilles tendon after repair in a sheep model. METHODS: Thirty sheep were randomly assigned into one of the six groups depending on the type of treatment received (PRGF or placebo) and survival time (2, 4 and 8 weeks). The Achilles tendon injury was repaired by suturing the tendinous edges employing a three-loop pulley pattern. A trans-articular external fixation system was then used for immobilization. The PRGF or placebo was administered on a weekly basis completing a maximum of three infiltrations. The force, section and tension values were compared between the operated and healthy Achilles tendons across all groups. RESULTS: The PRGF-treated tendons had higher force at 8 weeks compared with the placebo group (p = 0.007). Between 2 and 4 weeks, a significant increase in force in both the PRGF-treated tendon (p = 0.0027) and placebo group (p = 0.0095) occurred. No significant differences were found for section ratio between PRGF-treated tendons and the placebo group for any of the time periods evaluated. At 2 weeks, PRGF-treated tendons had higher tension ratio compared with placebo group tendons (p = 0.0143). Both PRGF and placebo treatments significantly improved the force (p < 0.001 and p = 0.0095, respectively) and tension (p = 0.009 and p = 0.0039, respectively) ratios at 8 weeks compared with 2 weeks. CONCLUSION: The application of PRGF increases Achilles tendon repair strength at 8 weeks compared with the use of placebo. The use of PRGF does not modify section and tension ratios compared with placebo at 8 weeks. The tension ratio progressively increases between 2 and 8 weeks compared with the placebo.

Comparison of the cardiopulmonary parameters after induction of anaesthesia with alphaxalone or etomidate in dogs.

OBJECTIVE: To compare the cardiorespiratory effects and quality of induction of and recovery from anaesthesia following etomidate or alphaxalone-HPCD IV. STUDY DESIGN: Randomized 'blinded' cross-over study. Twenty-four hours was allowed between phases. ANIMALS: Eight healthy adult Beagles (four male, four female). METHODS: Dogs were anaesthetized with sevoflurane for instrumentation, then allowed to awake. They then received etomidate (treatment E) or alphaxalone-HPCD (treatment A) intravenously to effect. Heart rate (HR), body temperature, invasive arterial pressures (AP), systemic vascular resistance index (SVRI), stroke volume index, cardiac index (CI), contractility, respiratory rate, central venous pressure, and capnometry were obtained before anaesthetic induction (baseline), 30 seconds and 1 minute after induction, after intubation, one minute after intubation, and for every 5 minutes afterwards until the dog began to swallow and the trachea was extubated. Arterial bloods were taken for analyses before induction, after intubation and every 10 minutes thereafter. The dogs breathed room air. The quality of induction of and recovery from anaesthesia were scored categorically. Statistical analyses used anova for repeated measures, paired t-tests or Wilcoxon signed rank-test as relevant. Significance was set at p < 0.05. RESULTS: The induction doses required were (mean ± SD) 2.91 ± 0.41 mg kg(-1) and 4.15 ± 0.7 mg kg(-1) for treatment E and A respectively. No significant changes in cardiovascular parameters were observed with treatment E. Treatment A resulted in statistically significant increases in HR and CI and reductions of APs and SVRI. Time to extubation was longer with treatment A (25 ± 7 minutes) than with treatment E (17 ± 4 minutes). Dogs became hypoxic with both treatments. The quality of induction and recovery were excellent with treatment A, but significantly less satisfactory with treatment E (recovery score, treatment E median 1, range 0-2; treatment A median 0, range 0-1). CONCLUSIONS AND CLINICAL RELEVANCE: Alphaxalone-HPCD caused significant tachycardia and increase in CI, and statistically (but not clinically) significant decreases in APs and SVRI. Etomidate caused no statistically significant cardiovascular changes. Quality of recovery was better with alfaxalone-HPCD. Both agents caused short-lived hypoxia, and oxygen supplementation is advisable.