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  • Author or Editor: Hiroshi Sakamoto x
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Abstract

Objective—To investigate the hemodynamic changes induced by injecting collagenase into the mitral valve to induce mitral valve regurgitation (MVR) in dogs.

Animals—9 healthy Beagles.

Procedure—Dogs were randomly assigned to 3 groups: control (saline [0.9% NaCl] solution; n = 3), single collagenase injection (C1; 3), and 2 collagenase injections (C2; 3). Open-heart surgery was performed, and saline or collagenase solutions were injected into the mitral valve. Before and weekly for 11 weeks after surgery, radiography, echocardiography, and phonocardiography were performed. Mean pulmonary arterial pressure and mean pulmonary arterial wedge pressure (mPAWP) were measured before and 11 weeks after surgery. Postmortem examinations were performed after dogs were euthanatized.

Results—No changes were detected in the control group during the 11-week follow-up period. A systolic murmur and MVR developed 1 week after surgery in groups C1 and C2. The murmur changed from a protosystolic to a pansystolic murmur, and left atrial diameter and the left atrial-to-aortic root diameter ratio increased with time. Mean pulmonary arterial pressure and mPAWP were greater 11 weeks after surgery in groups C1 and C2, compared with presurgery values. During necropsy, tissue loss was detected in the mitral valve at the site of collagenase injection. Degree of regurgitation corresponded to lesion size.

Conclusions and Clinical Relevance—Injection of collagenase into the mitral valve of healthy dogs induced MVR, and dogs with MVR developed progressive hemodynamic changes without acute overload. Collagenase-induced MVR may be an appropriate model for evaluation of prognostic markers of idiopathic MVR in dogs. (Am J Vet Res 2000;61:1593–1598)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate changes in canine hip joint characteristics during growth via computed tomography (CT) and compare CT features of hip joints with and without laxity in young dogs placed in 2 imaging positions.

Animals—21 dogs (42 hip joints).

Procedures—From 2 to 12 months after birth, CT examinations of the acetabulum of each hip joint in simulated normal standing and simulated weight-bearing positions were performed monthly for all dogs. Acetabular angle, dorsal acetabular rim angle (DARA), and femoral head diameter (FHd) were analyzed as skeletal variables; the lateral center edge angle (LCEA), dorsolateral subluxation (DLS) score, and center distance (CD) index were analyzed as joint laxity variables. At 12 months, all dogs underwent the Ortolani test to as-sess hip joint laxity.

Results—Hip joint laxity was detected in 5 dogs (10 joints) at 12 months of age; from 2 months, the acetabular angle and FHd increased and DARA decreased significantly until 5 months and the LCEA and DLS score increased significantly until 6 months. In nonlax hip joints in both positions, the CD index decreased significantly until 4 months of age and be-came stable thereafter. In lax hip joints, the CD index increased from 4 through 12 months; between 8 and 12 months, these changes were significantly greater in the weight-bearing position than in the standing position.

Conclusions and Clinical Relevance—Results suggest that CT-detected abnormalities in the DARA and CD index during body weight loading might be useful indicators of hip dysplasia in 2- to 6-month-old dogs.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To investigate the effects of polysulfated glycosaminoglycan (PSGAG) treatment on serum cartilage oligomeric matrix protein (COMP) concentration, matrix metal-loproteinase-2 (MMP-2) and -9 (MMP-9) activities, C-reactive protein (CRP) concentration, and lameness scores in dogs with osteoarthritis.

Animals—16 dogs with osteoarthritis and 5 clinically normal dogs.

Procedures—Dogs with osteoarthritis had a history of chronic lameness, and osteophytes were observed on radiographic evaluation of the affected joint. Polysulfated glycosaminoglycan was administered IM twice a week for a total of 8 treatments to all dogs with osteoarthritis and to clinically normal control dogs.

Results—Lameness scores after PSGAG treatment in osteoarthritic dogs improved in 12 of the 16 dogs. Serum COMP concentrations in osteoarthritic dogs were significantly higher than in control dogs before treatment. Lameness scores in osteoarthritic dogs decreased significantly after treatment, compared with before treatment. Lameness scores of 9 dogs with hind limb lameness improved significantly after treatment; these dogs had corresponding decreases in serum COMP concentrations. After treatment, serum COMP concentrations and lameness scores of 7 dogs with forelimb lameness remained high and were significantly higher than those of dogs with hind limb lameness. Serum MMP-9 activities of dogs with forelimb lameness were significantly higher than in dogs with hind limb lameness after treatment.

Conclusions and Clinical Relevance—IM administration of PSGAG inhibited COMP degradation in dogs with osteoarthritis. Results indicate that decreases in serum COMP concentrations might be related to improvement in lameness after PSGAG treatment.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To assay concentrations of cartilage oligomeric matrix protein (COMP) in canine sera and synovial fluid (SF), to compare COMP concentrations in clinically normal dogs and dogs with joint disease, and to analyze changes in COMP concentrations in dogs with experimentally induced acute synovitis.

Animals—69 control dogs without joint disease, 23 dogs with naturally occurring aseptic arthropathy, and 6 dogs with experimentally induced synovitis.

Procedure—Serum (n = 69) and SF (36) were obtained from control dogs. Samples of serum (n = 23) and SF (13) were obtained from dogs with naturally occurring aseptic arthropathy with or without radiographic features of osteoarthritis (OA). Serum and SF were obtained before and 1, 2, 3, and 7 days after induction of synovitis. The COMP concentrations were determined by use of an inhibition ELISA that had canine cartilage COMP and monoclonal antibody against human COMP.

Results—Concentrations of COMP in serum and SF of control dogs were 31.3 ± 15.3 and 298.7 ± 124.7 μg/ml, respectively. In naturally occurring OA, COMP concentrations in serum (44.9 ± 17.7 μg/ml) and SF (401.7 ± 74.3 μg/ml) were significantly higher than corresponding concentrations in control dogs. The COMP concentration in SF peaked 24 and 48 hours after induction of synovitis, whereas concentration in serum peaked on day 3.

Conclusions and Clinical Relevance—These results supported the hypothesis that COMP concentration in serum and SF of dogs may be altered after cartilage degradation or synovitis. Measurement of COMP concentrations can be useful when differentiating arthropathies in dogs. (Am J Vet Res 2002;63:598–603)

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in American Journal of Veterinary Research

Abstract

Objective

To elucidate the nature of ataxia observed in 3 cats spanning 2 generations.

Design

Experimental breeding was attempted to confirm heritability of the disease and establish the mode of inheritance; the original 3 cats and their offspring were studied.

Animals

Seven diseased cats spanning 3 generations and 11 neurologically normal cats.

Procedure

Cats were examined by use of the following methods: clinical observation, hematologic and serum biochemical examinations, neurologic examination, electrodiagnostics, magnetic resonance imaging, lysosomal enzyme activity assay, horizontal transmission test, and virologic and pathologic examinations.

Results

All kittens (1 male and 3 females) obtained by backcrosses developed pure cerebellar dysfunction from the age of 7 to 8 weeks onward. It became progressively worse, but not fatal, between 1 and 2.5 months. Prenatal or perinatal infection with feline panleukopenia virus, inherited lysosomal storage diseases, including gangliosidosis and mannosidosis, and feline hereditary neuroaxonal dystrophy were excluded. Magnetic resonance imaging indicated that size of the cerebellum of diseased cats was markedly reduced. Cerebellar cortical degeneration, especially with extensive destruction of Purkinje cells, was observed microscopically.

Conclusion

The disease was concluded to be cerebellar degeneration of a new clinical form in cats having an autosomal recessive mode of inheritance.

Clinical Relevance

When cerebellar dysfunction is diagnosed in a cat, hereditary cerebellar degeneration of this type should be considered in the differential diagnosis.(Am J Vet Res 1996; 57: 296-301)

Free access
in American Journal of Veterinary Research