PubMed · 8351041
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R A Dieter. 1993. Delayed hemorrhage.. https://pubmed.ncbi.nlm.nih.gov/8351041/
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STUDY DESIGN: Case report. OBJECTIVE: To illustrate a rare cause of thoracic spinal cord compression, its diagnosis, and its management. SUMMARY OF BACKGROUND DATA: Asymptomatic vertebral hemangiomas are common, but extraosseous extension causing spinal cord compression with neurologic symptoms is rare, and few cases appear in the English-language literature. METHOD: A previously asymptomatic 63-year-old man sought medical attention for acute back pain and thoracic myelopathy of 6 week's duration. Magnetic resonance imaging confirmed the presence of a mass in the T10 vertebral body with paravertebral and intracanalicular extension contributing to cord compression. Decompression and reconstructive surgery were performed and radiotherapy administered after surgery. Preoperative angiography was not performed because of the patient's rapidly progressive neurologic deterioration and the consideration that the differential diagnosis of vertebral hemangioma was less likely. RESULTS: The diagnosis of benign capillary hemangioma was made histologically. Neurologic recovery was complete except for minor residual sensory changes in the legs. At follow-up 10 months after surgery the patient had returned to his usual active life and motor mower repairing business. CONCLUSION: Extraosseous extension of vertebral hemangiomas is a rare cause of thoracic spinal cord compression. As such, the available data are derived from reports based on series involving only a small number of cases, rather than on results of randomized controlled trials. Those causing progressive neurologic symptoms should be surgically decompressed, with the specific procedure determined by the extent and site of the lesion. Preoperative angiography is recommended, but embolization is not always necessary or even possible. Postoperative radiotherapy is recommended when tumor removal is subtotal.
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This study was conducted to examine segmental differences in vasodilatation caused by the basal release of nitric oxide (NO) in the serially connected pulmonary vessels and to estimate the relative contributions of endothelial and neuronal NO synthase (NOS), and inducible NOS to the vasodilatation. Using an X-ray TV system on in vivo cat lungs, we measured internal diameter (ID) changes in resistance (100-400 microm ID), small conduit (600-1000 microm) and large conduit (1200-1700 microm) arteries, and veins of the same size. Non-selective NOS inhibitors, L-NAME (30-50 mg/kg i.v.) and L-NMMA (40-60 mg/kg i.v.), decreased the ID of all vessels studied, although their D-isomers had no effect. The decrease was larger in conduit arteries than in resistance arteries, with maximum response of small conduit arteries (25 +/- 2%), while venous segments displayed relatively uniform response (10-12%). L-Arginine completely abolished the ID decrease but hexamethonium bromide and phentolamine had no effect. Selective inhibitors of inducible NOS, L-canavanine (100 mg/kg i.v.) and S-methylisothiourea (10 mg/kg i.v.) did not affect any of the vessels. The data suggest that basal release of NO chiefly derived from endothelial NOS serves to dilate cat pulmonary arteries and veins, particularly small conduit arteries.