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
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)
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.
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.
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
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)
Objective—To evaluate changes in serum cartilage oligomeric matrix protein (COMP) concentrations in response to exercise in horses.
Animals—15 horses in experiment 1 and 27 horses in experiment 2.
Procedures—In experiment 1, 15 Thoroughbreds free of orthopedic disease underwent a standardized exercise protocol. Running velocity and heart rate (HR) were recorded, and blood samples were collected immediately before (baseline) and 1, 5, and 24 hours after a single episode of exercise. In experiment 2, 27 horses underwent 9 stages of a training program in which each stage consisted of 4 to 8 consecutive daily workouts followed by a rest day. Blood samples were collected immediately before the first and final daily workouts in each stage. Serum COMP concentrations were measured via inhibition ELISA with a monoclonal antibody (14G4) against equine COMP.
Results—In experiment 1, mean serum COMP concentration was significantly higher than baseline 1 and 5 hours after exercise and returned to baseline concentrations 24 hours after exercise. Mean serum baseline COMP concentration increased as the velocity of running at maximum HR and at an HR of 200 beats/min increased, being significantly higher during the third and fourth exercise tests than during the first. In experiment 2, mean baseline COMP concentration at the final workout of each stage was significantly higher than that at the first workout, beginning with stage 3.
Conclusions and Clinical Relevance—Serum COMP concentrations changed significantly in response to exercise. Exercise may enhance movement of COMP into the circulation as well as change the basal turnover rate of COMP.