Platelet function in dogs with chronic liver disease.

OBJECTIVES: To assess platelet function, buccal mucosal bleeding time and plasma von Willebrand factor concentration in dogs with chronic inflammatory and/or fibrotic liver disease and to compare results with those obtained in healthy dogs. MATERIALS AND METHODS: Preliminary study including 18 dogs with chronic inflammatory and/or fibrotic liver disease undergoing liver biopsy and 18 healthy age-matched control dogs. Platelet function was assessed by measuring closure time with the PFA-100® analyser using adenosine diphosphate (ADP) as an agonist. Buccal mucosal bleeding time, closure time and plasma von Willebrand factor antigen were measured in dogs in both groups. After undergoing ultrasound-guided needle biopsy, dogs were monitored for haemorrhage to determine if there was an association of any measurement with post-biopsy bleeding. RESULTS: The closure time was not different between the liver disease group (median 76.3; range 53 to 118.5 seconds) and control group (72.8; 57 to 89.5 seconds). The buccal mucosal bleeding time was longer in the liver disease group (median 138; range 95 to 229 seconds) than the control group (103; 63 to 200 seconds). The plasma von Willebrand factor antigen concentration was not different between the liver disease group (median 203; range 109 to 351%) and control group (165.5; 63 to 246%). CLINICAL SIGNIFICANCE: In this study, dogs with chronic necroinflammatory and/or fibrotic liver disease did not have overt, clinically relevant derangements in platelet function as assessed by buccal mucosal bleeding time, closure time and von Willebrand factor analysis. In addition, none of the dogs undergoing percutaneous ultrasound-guided biopsy in the study exhibited bleeding complications post-biopsy procedure.

Extracorporeal shockwave therapy raises mechanical nociceptive threshold in horses with thoracolumbar pain.

BACKGROUND: Although extracorporeal shockwave therapy (ESWT) is a common treatment for horses with back pain, effects on mechanical nociceptive threshold (MNT) and multifidus muscle cross sectional area (CSA) in the spine are unknown. OBJECTIVES: To evaluate effects of ESWT on spinal MNT and multifidus muscle CSA in horses with thoracolumbar pain. STUDY DESIGN: Non-randomised trial. METHODS: Thoracolumbar spines of 12 horses with thoracolumbar pain were radiographed to document existing pathology. Each horse received three ESWT treatments, 2 weeks apart (days 0, 14, 28). Palpation scores were documented (days 0, 45 and 65). Ultrasonographic CSA of left and right multifidus muscles was recorded at T12, T14, T16, T18, L3 and L5 (days 0, 45 and 65). MNT was measured at the same spinal sites every 7 days (day 0-56). RESULTS: Mechanical nociceptive threshold in 10/12 horses (83%) was greater at each time point compared with day 0 (P < 0.05). Mechanical nociceptive threshold increased at all time points at six sites in 2/12 (16%), at five sites in 3/12 (25%), at four sites in 4/12 (33%) and at one site in 1/12 (8%; P < 0.05). Mechanical nociceptive threshold average per cent  increase from day 0 to 56 was 64% for the thoracic region (T12-T18) and 29% for the lumbar region (L3-L5). There was no statistical difference in MNT from day 35 to 56 (P = 0.25). A bimodal analgesic trend was observed following ESWT. Degree of radiographic change was not associated with response to treatment. No significant change in multifidus muscle CSA was observed. MAIN LIMITATIONS: Small study size and lack of control group. CONCLUSIONS: Three treatments of ESWT 2 weeks apart raised MNT over a 56-day period in horses with back pain, but did not influence change in CSA of the multifidus muscle. While ESWT appears justifiable for analgesia, physiotherapeutic techniques may be necessary in conjunction for concurrent muscle rehabilitation.

Prevalence of hyoid injuries in dogs and cats undergoing computed tomography.

Fractures of the hyoid bones have been reported occasionally in dogs, but the prevalence and significance of hyoid injury in dogs and cats are unknown. In human beings, hyoid injury is rare and usually is caused by direct trauma to the greater cornu, which are analogous to the paired canine and feline thyrohyoid bones. The aim of this study was to describe the prevalence and morphology of hyoid bone injury detected in dogs and cats undergoing computed tomography (CT) for unrelated disease. CT studies of 293 dogs and 100 cats from 2012 to 2016 were identified and reviewed retrospectively. Hyoid fracture (total of eight bones) or luxation (total of four sites) was present in 9/293 (3.1%) dogs, but none of the cats. One dog had bilateral fractures and one dog had bilateral luxations. The most frequently fractured bone was the epihyoid bone (4/8 fractures). Fracture margins were tapered and sclerotic, consistent with chronic non-union. There was no history of trauma, dysphagia or dyspnea in 7/9 dogs with hyoid fractures. Hyoid bone injury, particularly epihyoid bone fracture, may be an incidental finding in dogs.

Comparison of autogenous cancellous bone grafting and extracorporeal shock wave therapy on osteotomy healing in the tibial tuberosity advancement procedure in dogs. Radiographic densitometric evaluation.

OBJECTIVES: To compare optical values in the osteotomy gap created after a tibial tuberosity advancement (TTA) treated with autogenous cancellous bone graft, extracorporeal shock wave therapy, a combination of autogenous cancellous bone graft and extracorporeal shock wave therapy, and absence of both autogenous cancellous bone graft and extracorporeal shock wave therapy using densitometry. METHODS: Dogs that were presented for surgical repair of a cranial cruciate ligament rupture were randomly assigned to one of four groups: TTA with autogenous cancellous bone graft (TTA-G), TTA with autogenous cancellous bone graft and extracorporeal shock wave therapy (TTA-GS), TTA with extracorporeal shock wave therapy (TTA-S), and TTA with no additional therapy (TTA-O). Mediolateral radiographs at zero, four and eight weeks after surgery were evaluated to compare healing of the osteotomy gap via densitometry. An analysis of variance was used to compare the densitometric values between groups. RESULTS: At four weeks after surgery, a significant difference in osteotomy gap density was noted between TTA-GS (8.4 millimetres of aluminium equivalent [mmAleq]) and TTA-S (6.1 mmAleq), and between TTA-GS (8.4 mmAleq) and TTA-O (6.4 mmAleq). There were no significant differences noted between any groups at the eight week re-evaluation. CLINICAL SIGNIFICANCE: There were no significant differences in the osteotomy gap density at eight weeks after surgery regardless of the treatment modality used. The combination of autogenous cancellous bone graft and extracorporeal shock wave therapy may lead to increased radiographic density of the osteotomy gap in the first four weeks after surgery. Densitometry using an aluminium step wedge is a feasible method for comparison of bone density after TTA in dogs.

Simvastatin and GGTI-2133, a geranylgeranyl transferase inhibitor, increase erythrocyte deformability but reduce low O(2) tension-induced ATP release.

Statin drugs inhibit 3-hydroxy-3-methylglutaryl CoA reductase, which reduces the synthesis of both cholesterol and isoprenoids (geranylgeranyl pyrophosphate and farnesyl pyrophosphate), with the latter being lipid molecules responsible for the posttranslational modification of small GTP-binding proteins such as Rho. Effects of statins, independent of lowering blood cholesterol levels, are thought to occur by inhibition of Rho/Rho kinase. The Rho kinase inhibitor Y-27632 has been reported to increase both erythrocyte deformability and low O2 tension-induced ATP release. Here, we tested the hypothesis that by inhibiting Rho/Rho kinase, simvastatin would increase both erythrocyte deformability and low O2 tension-induced ATP release. Male Sprague-Dawley rats were divided into two groups, control or simvastatin treated [simvastatin-supplemented chow (0.02%)], for 4 wk. Simvastatin treatment increased rat erythrocyte deformability compared with controls (n = 6, P < 0.05). However, erythrocytes of simvastatin-treated rats (n = 9, P < 0.05) exhibited impaired low O2 tension-induced ATP release. Similarly, the geranylgeranyl transferase inhibitor GGTI-2133 (10 µM) also increased deformability and impaired low O2 tension-induced ATP release in healthy human erythrocytes (P < 0.05). Interestingly, ATP release in response to mastoparan 7 (n = 7, P < 0.05), which directly activates Gi, and isoproterenol (n = 5, P < 0.05), which signals through Gs, was not altered by incubation with GGTI-2133. These results suggest that although statins increase erythrocyte deformability, likely by inhibiting geranylgeranylation, the finding that both statins and a geranylgeranyl transferase inhibitor attenuated low O2 tension-induced ATP release demonstrates that factors in addition to erythrocyte deformability are critical for ATP release in response to this physiological stimulus.

Cytolethal distending toxin promotes Helicobacter cinaedi-associated typhlocolitis in interleukin-10-deficient mice.

Helicobacter cinaedi colonizes a wide host range, including rodents, and may be an emerging zoonotic agent. Colonization parameters, pathology, serology, and inflammatory responses to wild-type H. cinaedi (WT(Hc)) were evaluated in B6.129P2-IL-10(tm1Cgn) (IL-10(-/-)) mice for 36 weeks postinfection (WPI) and in C57BL/6 (B6) mice for 12 WPI. Because cytolethal distending toxin (CDT) may be a virulence factor, IL-10(-/-) mice were also infected with the cdtB(Hc) and cdtB-N(Hc) isogenic mutants and evaluated for 12 WPI. Consistent with other murine enterohepatic helicobacters, WT(Hc) did not cause typhlocolitis in B6 mice, but mild to severe lesions developed at the cecocolic junction in IL-10(-/-) mice, despite similar colonization levels of WT(Hc) in the cecum and colon of both B6 and IL-10(-/-) mice. WT(Hc) and cdtB mutants also colonized IL-10(-/-) mice to a similar extent, but infection with either cdtB mutant resulted in attenuated typhlocolitis and hyperplasia compared to infection with WT(Hc) (P < 0.03), and only WT(Hc) infection caused dysplasia and intramucosal carcinoma. WT(Hc) and cdtB(Hc) mutant infection of IL-10(-/-) mice elevated mRNA expression of tumor necrosis factor alpha, inducible nitric oxide synthase, and gamma interferon in the cecum, as well as elevated Th1-associated serum immunoglobulin G2a(b) compared to infection of B6 mice (P < 0.05). Although no hepatitis was noted, liver samples were PCR positive at various time points for WT(Hc) or the cdtB(Hc) mutant in approximately 33% of IL-10(-/-) mice and in 10 to 20% of WT(Hc)-infected B6 mice. These results indicate that WT(Hc) can be used to model inflammatory bowel disease in IL-10(-/-) mice and that CDT contributes to the virulence of H. cinaedi.