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- Author or Editor: Takashi Takeuchi x
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Objective—To determine whether angiogenesis and microglial activation were related to seizure-induced neuronal death in the cerebral cortex of Shetland Sheepdogs with familial epilepsy.
Animals—Cadavers of 10 Shetland Sheepdogs from the same family (6 dogs with seizures and 4 dogs without seizures) and 4 age-matched unrelated Shetland Sheepdogs.
Procedures—Samples of brain tissues were collected after euthanasia and then fixed in neutral phosphate–buffered 10% formalin and routinely embedded in paraffin. The fixed samples were sectioned for H&E staining and immunohistochemical analysis.
Results—Evidence of seizure-induced neuronal death was detected exclusively in samples of cerebral cortical tissue from the dogs with familial epilepsy in which seizures had been observed. The seizure-induced neuronal death was restricted to tissues from the cingulate cortex and sulci surrounding the cerebral cortex. In almost the same locations as where seizure-induced neuronal death was identified, microvessels appeared longer and more tortuous and the number of microvessels was greater than in the dogs without seizures and control dogs. Occasionally, the microvessels were surrounded by oval to flat cells, which had positive immunohistochemical results for von Willebrand factor. Immunohistochemical results for neurons and glial cells (astrocytes and microglia) were positive for vascular endothelial growth factor, and microglia positive for ionized calcium–binding adapter molecule 1 were activated (ie, had swollen cell bodies and long processes) in almost all the same locations as where seizure-induced neuronal death was detected. Double-label immunofluorescence techniques revealed that the activated microglia had positive results for tumor necrosis factor-α, interleukin-6, and vascular endothelial growth factor receptor 1. These findings were not observed in the cerebrum of dogs without seizures, whether the dogs were from the same family as those with epilepsy or were unrelated to them.
Conclusions and Clinical Relevance—Signs of angiogenesis and microglial activation corresponded with seizure-induced neuronal death in the cerebral cortex of Shetland Sheepdogs with familial epilepsy. Microglial activation induced by vascular endothelial growth factor and associated proinflammatory cytokine production may accelerate seizure-induced neuronal death in dogs with epilepsy.
Objective—To investigate the effect of topical application of undiluted lavender oil on sympathovagal activity in dogs.
Animals—5 healthy adult male Beagles.
Procedures—An ambulatory ECG monitor (Holter recorder) was placed on each dog (day0), and 48-hour ECGs were recorded, beginning at 8:00 the next day (day 1). Lavender oil (0.18 mL) or saline (0.9% NaCl) solution (0.18 mL) was topically applied to the inner pinnas of both ears of all dogs at 8:30, 12:00, 15:30, and 19:00 on day 2. Each trial was duplicated in each dog, with an interval of 3 to 4 days between trials. Spectral indices of heart rate variability, power in the high-frequency range, and the ratio of low-frequency to high-frequency power were calculated as an indirect estimate of autonomic nerve activity.
Results—When dogs were treated with lavender oil, the mean heart rate was significantly lower during the period of 19:00 to 22:30 on day 2, compared with the mean heart rate during the same period when dogs were treated with saline solution. On the other hand, high-frequency power during the period of 15:30 to 19:00 was significantly higher when dogs were treated with lavender oil, compared with the high-frequency power during the same period when dogs were treated with saline solution.
Conclusions and Clinical Relevance—The study revealed some evidence that topical application of lavender oil affected vagal activity in dogs. However, whether such an effect exists and whether lavender oil has a calming effect on dogs remains equivocal and requires additional investigation.
Objective—To determine whether mitral valve repair (MVR) under cardiopulmonary bypass would be an effective treatment for mitral regurgitation in small-breed dogs.
Design—Retrospective case series.
Animals—48 small-breed dogs (body weight, 1.88 to 4.65 kg [4.11 to 10.25 lb]; age, 5 to 15 years) with mitral regurgitation that underwent surgery between August 2006 and August 2009.
Procedures—Cardiopulmonary bypass was performed with a cardiopulmonary bypass circuit. After induction of cardiac arrest, a mitral annuloplasty was performed, and the chordae tendineae were replaced with expanded polytetrafluoroethylene chordal prostheses. After closure of the left atrium and declamping to restart the heart, the thorax was closed.
Results—Preoperatively, cardiac murmur was grade 3 of 6 to 6 of 6, thoracic radiography showed cardiac enlargement (median vertebral heart size, 12.0 vertebrae; range, 9.5 to 14.5 vertebrae), and echocardiography showed severe mitral regurgitation and left atrial enlargement (median left atrium-to-aortic root ratio, 2.6; range, 1.7 to 4.0). 45 of 48 dogs survived to discharge. Three months after surgery, cardiac murmur grade was reduced to 0/6 to 3/6, and the heart shadow was reduced (median vertebral heart size, 11.1 vertebrae, range, 9.2 to 13.0 vertebrae) on thoracic radiographs. Echocardiography confirmed a marked reduction in mitral regurgitation and left atrium-to-aortic root ratio (median, 1.7; range, 1.0 to 3.0).
Conclusions and Clinical Relevance—We successfully performed MVR under cardiopulmonary bypass in small-breed dogs, suggesting this may be an effective surgical treatment for dogs with mitral regurgitation. Mitral valve repair with cardiopulmonary bypass can be beneficial for the treatment of mitral regurgitation in small-breed dogs.