Chronic tissue ischemia due to defective vascular perfusion is a hallmark feature of peripheral artery disease for which minimal therapeutic options exist. We have reported that sodium nitrite therapy exerts cytoprotective effects against acute ischemia/reperfusion injury in both heart and liver, consistent with the model of bioactive NO formation from nitrite during ischemic stress. Here, we test the hypothesis that chronic sodium nitrite therapy can selectively augment angiogenic activity and tissue perfusion in the murine hind-limb ischemia model. Various therapeutic doses (8.25-3,300 g/kg) of sodium nitrite or PBS were administered. Sodium nitrite significantly restored ischemic hind-limb blood flow in a timedependent manner, with low-dose sodium nitrite being most effective. Nitrite therapy significantly increased ischemic limb vascular density and stimulated endothelial cell proliferation. Remarkably, the effects of sodium nitrite therapy were evident within 3 days of the ischemic insult demonstrating the potency and efficacy of chronic sodium nitrite therapy. Sodium nitrite therapy also increased ischemic tissue nitrite and NO metabolites compared to nonischemic limbs. Use of the NO scavenger carboxy PTIO completely abolished sodium nitrite-dependent ischemic tissue blood flow and angiogenic activity consistent with nitrite reduction to NO being the proangiogenic mechanism. These data demonstrate that chronic sodium nitrite therapy is a recently discovered therapeutic treatment for peripheral artery disease and critical limb ischemia.wound healing ͉ endothelial cell ͉ nitric oxide ͉ peripheral artery disease ͉ tissue perfusion

Twenty-eight surgical procedures were performed in 23 dogs with atlantoaxial subluxation. Dorsal stabilization in seven dogs resulted in two recoveries and five failures of fixation. Ventral decompression and stabilization in 18 dogs resulted in eight recoveries and four failures of fixation. Six dogs died or were euthanatized within 7 days of ventral stabilization. Using either technique, four of seven nonambulatory dogs recovered.

In the present study, presence of aplastic or hypoplastic articular processes in the thoracolumbar region did not always produce neurologic signs. However, fibrous constrictive myelopathy should be considered in Pugs with pelvic limb gait and postural reaction deficits and lack of hyperpathia upon palpation of the vertebral column. Additional studies are warranted to further characterize the disease process and determine the most effective means of treatment.

In a three-year prospective study, computed tomographic (CT) and surgical findings were compared for nine large breed dogs with lumbosacral stenosis. Surgically-excised tissue was examined histologically in seven dogs and additional necropsy evaluation was performed in one dog. The CT ahnormalities observed at sites of confirmed cauda equina compression were: loss of epidural fat, increased soft tissue opacity, bulging of the intervertebral disc margin, spondylosis, thecal sac displacement, narrowed intervertebral foramen, narrowed vertebral canal, thickened articular process, articular process subluxation, articular process osteophyte, and telescoped sacral lamina. The CT characteristics of lumbosacral degenerative disease and discospondylitis were similar to those described in humans. In three dogs, CT findings at the site of cauda equina compression were consistent with congenital or developmental spinal stenosis, but the method of surgical exposure precluded confirmation. Epidural fibrosis (eight dogs) and multi-level CT abnormalities (six dogs) were identified but the cause@) and significance were unknown.

The brains of 23 canine patients and six random-source dogs were examined ultrasonographically through the bregmatic fontanelle or a surgical craniotomy. Fifteen dogs had abnormal neurologic signs; the others were normal on neurologic examination. Untrasound results were compared with signalment, clinical signs, electroencephalography, computed tomography, radiology and histopathology. The purposes of the study were to demonstrate the use of ultrasound for the diagnosis of canine hydrocephalus and to determine whether there is a relationship between ventricular size and clinical signs. Lateral ventricles were considered enlarged if lateral ventricular height, ventricle-mantle ratio, or ventricle-hemisphere ratio, at the level of or caudal to the interthalamic adhesion in the transverse plane, exceeded 0.35 cm, 0.25 or 0.19, respectively. Of the 29 dogs examined, 14 had enlarged lateral ventricles and abnormal neurologic signs. Five dogs had enlarged lateral ventricles but appeared neurologically normal (occult hydrocephalus). Correlation was poor between ventricular size and clinical signs.