To characterize ocular findings in hypertensive dogs, determine prevalence of hypertension in dogs with ocular disease suggestive of hypertension, and examine possible relationships between degree of hypertension and ocular disease.
Retrospective case series.
65 dogs initially referred for blood pressure measurement (n = 22), ophthalmic examination (25), or both (18).
Medical records were reviewed to identify dogs examined at the teaching hospital that underwent a complete ophthalmic examination and blood pressure measurement within a 24-hour period between January 1, 2005, and December 31, 2007. Signalment, history, blood pressure measurements, ophthalmic examination findings, and any vasoactive drug treatments were recorded. Ocular lesions considered likely to be associated with systemic hypertension included retinal hemorrhage, retinal detachment, hyphema, tortuous vessels, and subretinal edema.
Of the 65 dogs, 42 were hypertensive (systolic blood pressure ≥ 160 mm Hg) and 23 were normotensive. Sixty-two percent (26/42) of hypertensive dogs had ≥ 1 type of ocular lesion identified. Retinal hemorrhage was the most common ocular lesion in hypertensive dogs (17/42 [40%]). The presence of ≥ 1 type of ocular lesion had moderate sensitivity and specificity of 62% and 61 %, respectively, for identification of hypertension. Fifteen of the 25 (60%) dogs referred for blood pressure measurement after initial ophthalmic examination were found to be hypertensive.
Ocular lesions are common in dogs with systemic hypertension. Dogs with hypertension or diseases associated with hypertension should be monitored carefully for evidence of ocular target organ damage, and hypertension should be systematically ruled out in dogs with characteristic ocular lesions.
"Vitreous hemorrhage, which can occur in beagle dogs as a
spontaneous variant, is most frequently caused by trauma, or a systemic clotting disorder,
and can occur secondary to retinal detachment, which is often associated with increased
ocular pressure. Retinal hemorrhage is induced by compounds acting directly or indirectly on
the clotting mechanisms, e.g., coumarin anticoagulants22 and is the most common ocular lesion in dogs with systemic
hypertension36. The SSRIs and
serotonin and norepinephrine re-uptake inhibitors (SNRIs) drugs have effects on
cardiovascular and coagulation mechanisms. Increases in heart rate and blood pressure have
been seen clinically with fluoxetine overdose. "
[Show abstract][Hide abstract] ABSTRACT: AZD3783, a cationic amphiphilic drug and a potent inhibitor of the 5-hydroxytryptamine (5-HT1B) receptor, was explored as a potential treatment for depression. To support clinical trials, repeat dose toxicity studies in rats and dogs were conducted. Here we report toxicity findings in dogs after dosing from 1 to 3 months. In the 1-month study, there were minimal neuronal vacuolation in the brain, a marked increase in liver enzymes accompanied by hepatocellular degeneration/necrosis and phospholipidosis (PLD), and PLD/cholecystitis in the gallbladder of animals dosed at 47 mg/kg/day. In the 3-month study, neurotoxicity resulted in euthanasia of one animal dosed at 30 mg/kg/day after 86 days. Extensive pathologic changes were seen in all animals in retina epithelium (inclusion bodies), brain (neuronal vacuolation, degeneration, or necrosis and nerve fiber degeneration), spinal ganglia (vacuolation, degeneration, or necrosis), as well as sciatic and optic nerves (degeneration). Pigment-laden macrophages were observed in the lung, kidney, liver, gallbladder, bone marrow, gastrointestinal tract, and lymphoid tissues. Also seen were vitrel and retinal hemorrhage in the eyes. A brain concentration and pathology study showed that the concentration of AZD3783 in the brain was approximately 4 times higher than in the plasma after 4 weeks of dosing, however, they were similar in all regions examined, and did not correlate with areas with pathologic findings. Our findings with AZD3783 in dogs have not been reported previously with other CNS compounds that effect through serotonergic pharmacology.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.