Hypercoagulability and ACTH-dependent hyperadrenocorticism in dogs.

BACKGROUND: Dogs with hyperadrenocorticism are at risk of thromboembolic disease, which might be caused by an underlying hypercoagulable state. HYPOTHESIS/OBJECTIVES: To assess hemostatic function in dogs with ACTH-dependent hyperadrenocorticism (ADHAC) before and after treatment. ANIMALS: Nineteen dogs with ADHAC and 40 normal dogs. METHODS: Prospective, observational study. Dogs with ADHAC were recruited from the referral hospital patient population; normal dogs were recruited from staff and students at the study's institution. Hemostasis was assessed before and at 3 and 6 months after treatment with trilostane (T0, T3, T6) by kaolin-activated thrombelastography with platelet mapping (TEG-PM), prothrombin time, activated partial thromboplastin time, fibrinogen concentration, and antithrombin activity (AT). RESULTS: Dogs with ADHAC had statistically significantly increased α-angle (P < .01) and maximum amplitude (MA)(thrombin) (P < .01) on TEG-PM, and significantly decreased κ (P < .005) at T0, T3, and T6. Platelet count (P < .001) and fibrinogen concentration (P < .001), but not AT activity, were increased in dogs with ADHAC at T0, T3, and T6. CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with ADHAC have thrombelastographic evidence of hypercoagulability and remained hypercoagulable during treatment. AT deficiency does not appear to be involved in the pathogenesis of hypercoagulability in this population.

Sacral osteochondrosis in two German Shepherd Dogs.

Two young adult male castrated German Shepherd Dogs were referred for evaluation of intermittent episodes of hindlimb pain. Physical examination suggested lumbosacral stenosis, and plain radiographs and computed tomography revealed lesions consistent with sacral osteochondrosis. One dog had osteochondral fragments removed surgically; the other was managed conservatively. The surgically treated dog had complete resolution of clinical signs whereas the dog managed conservatively had repeated episodes of mild pain and received one short course of non-steroidal anti-inflammatory medication in 18 months. Sacral osteochondrosis has not been previously reported in Australia.

The beneficial effect of nicardipine on the healing of myocardial infarcts in dogs.

The effect of 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylic acid 3-[2-(N-benzyl-N-methyl amino)] ethyl ester 5-methyl ester hydrochloride (nicardipine, RS-69216, YC-93), on the healing of myocardial infarcts has been examined in dogs surviving for 3 months after ligation of the left anterior descending coronary artery (LAD). Three groups of 12-14 dogs were subjected to the following treatments: a) Group X received one-month oral pretreatment (1-2 mg/kg/d) with post-ligation i.v. treatment delayed for 1 h (10 micrograms/kg followed by 2 micrograms/kg/15 min for 5 h) and oral treatment (1-2 mg/kg/d) for 3 months (n = 9 survivors). b) Group Y received oral placebo for one month, i.v. saline vehicle every 15 min for 5 h commencing 1 h postligation, and oral placebo for 3 months (n = 8 survivors). c) Group Z received oral placebo for one month as in group Y, i.v. and oral drug treatment post-ligation as for group X (n = 10 survivors). Recordings were made of general haemodynamics and at post mortem, each heart was X-rayed and sliced transversely to give 14 sections from which detailed observations were made on left ventricular (LV) geometry. Comparative morphological measurements were available from filed data for 11 normal dog hearts (designated group C) of similar type. Nicardipine treatment significantly modified the general haemodynamic responses to LAD ligation particularly in maintaining a low LV systolic pressure and inhibiting elevation of LV end diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)