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Bladder outlet obstruction (BOO) may lead to detrusor decompensation through progressive bladder remodeling. Most experimental studies rely on acutely induced BOO in rodents. Since progressive obstruction better reflects the condition, non-lethal models are needed to investigate chronic obstruction pathophysiology and evaluate regenerative therapies. This exploratory study aimed to evaluate (1) a progressive BOO model induced by an artificial urethral sphincter (AUS) in 2 dogs and (2) the systemic administration of autologous adipose-derived mesenchymal stem cells (ADMSCs) after obstruction release. Two intact male dogs underwent progressive BOO through gradual AUS inflation. Longitudinal assessment included telemetric urodynamic monitoring, urethral pressure profilometry, ultrasonography, post-void residual measurement, oxidative stress markers in serial blood samples and serial bladder biopsies for histology, transmission electron microscopy, immunohistochemistry, RT-qPCR and RNA sequencing (CCL2, CCR2, GFAP, VEGF, HGF). After AUS removal, one dog received three intravenous injections of 20 × 106 PKH26-labelled autologous ADMSCs. BOO induced functional changes (increased detrusor pressure and urethral resistance, decreased urinary flow, prolonged voiding). No detrusor decompensation or fibrosis comparable to the human condition developed, encouraging refinement of this model. ADMSCs appeared to reach the bladder wall safely, but any influence on the glutathione redox system and CCL2 protein expression needs to be confirmed.

Regenerative therapy for bladder diseases has been studied in rodent to restore bladder function after a chronic and irreversible bladder wall deterioration. These studies rarely demonstrate the presence of stem cells in the bladder. Cell-tracking after intravenous (IV) administration of stem cells enables to confirm the homing potential of an injury. Our objective was to assess, in one dog, the homing capability of autologous adipose-derived mesenchymal stromal/stem cells (ADMSCs) injected intravenously to an acute bladder injury. Adipose-derived mesenchymal stromal/stem cells were isolated from the subcutaneous tissue of a dog and labelled. As a homing signal, a full-thickness bladder biopsy representing an acute injury was created in this dog (day 0, control time). Twenty million autologous PKH26-labelled ADMSCs were injected in the cephalic vein on days 1, 4 and 8. Urinalysis was performed (day 5). Bladder biopsy was repeated at the location of the previous scar to assess the presence of labelled ADMSCs in the bladder wall (day 10). Labelled ADMSCs were observed in the second bladder biopsy, not in the initial biopsy nor in urine. The only adverse event mild, self-limiting hematuria. Complete cell blood count, blood urea nitrogen and plasma creatinine were within normal limits (day 5). The comparison of bladder biopsies before and after IV administration of autologous ADMSCs indicates that they reached the bladder injury. Our protocol was feasible and safe. Hematuria was probably due to the bladder biopsy. These results could encourage the evaluation of this protocol in larger cohorts of dogs.

While oxidative stress has been studied in pathologic conditions in dogs, data in presumably healthy dogs and standardized protocols are lacking. This work purposed to bridge the gap by presenting provisional physiological ranges for oxidative stress biomarkers in a group of Beagle dogs. Based on our long-standing clinical expertise in the field of oxidative stress, nine plasma biomarkers of oxidative stress were evaluated for their concentrations (mean ± SD) in 14 healthy adult Beagle dogs. Selected biomarkers were: vitamins C (7.90 ± 1.36 μg/mL) and E (34.1 ± 6.63 μg/mL), zinc (0.80 ± 0.17 mg/L), copper (0.54 ± 0.048 mg/L), selenium (256 ± 25.7 μg/L), total and oxidized glutathione (822 ± 108 μM and 3.56 ± 1.76 μM), myeloperoxidase (67.4 ± 56.2 ng/mL), and isoprostanes (340 ± 95.3 ng/mL). Glutathione peroxidase activity and superoxide anion production in whole blood were also measured. Glutathione peroxidase activity was 473 ± 34.0 IU/g of hemoglobin and superoxide anion production in whole blood was 18,930 ± 12,742 counts per 30 min. Reduced glutathione/oxidized glutathione and copper/zinc ratios were, respectively, 280 ± 139 and 0.70 ± 0.15. Sex-related differences were recorded for zinc ( = 0.0081), copper/zinc ratio ( = 0.0036) and plasma isoprostanes ( = 0.0045). Provisional physiological norms covering 95% of our group were proposed for each biomarker and should be of interest for future studies of canine oxidative stress.

Catheter fragment embolism is a potential complication of peripheral venous catheterisation. A three-year-old male dachshund was treated for a tibial fracture. The anaesthesia, orthopaedic procedure and hospitalisation recovery were uneventful. At the time of venous catheter removal, its breakage was noticed. A catheter tip embolisation was suspected and confirmed in the cephalic vein with radiography and ultrasound. A tourniquet was immediately applied proximally to the elbow. It prevented the catheter tip from further migration and central embolisation. A longitudinal venotomy of the cephalic vein allowed the removal of the fragment. Stitches were removed 10 days later and clinical examination was normal.