Effects of arterial ischemia and venous congestion on the lumbar nerve root in dogs

The development of radiculopathy in patients with lumbar canal stenosis is thought to be closely related to intraradicular edema resulting from compression. However, there is little agreement as to question which is more essential for intermittent claudication: ischemia or congestion. The aim of the...

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Published in:	Journal of orthopaedic research Vol. 26; no. 11; pp. 1533 - 1540
Main Authors:	Kobayashi, Shigeru, Takeno, Kenichi, Miyazaki, Tsuyoshi, Kubota, Masafumi, Shimada, Seichior, Yayama, Takafumi, Uchida, Kenzo, Normura, Eiki, Mwaka, Erisa, Baba, Hisatoshi
Format:	Journal Article
Language:	English
Published:	Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-11-2008
Subjects:	Animals Aorta blood flow Blood Pressure Blood-Nerve Barrier - ultrastructure Disease Models, Animal Dogs Hyperemia - pathology intermittent claudication Intermittent Claudication - physiopathology Ischemia - pathology lumbar canal stenosis Nerve Compression Syndromes - pathology nerve root Neural Conduction Radiculopathy - pathology Spinal Nerve Roots - pathology Spinal Nerve Roots - physiopathology Vena Cava, Inferior venous congestion
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Summary:	The development of radiculopathy in patients with lumbar canal stenosis is thought to be closely related to intraradicular edema resulting from compression. However, there is little agreement as to question which is more essential for intermittent claudication: ischemia or congestion. The aim of the present experimental investigation was to examine the effect of ischemia and congestion on the nerve root using dogs. The aorta was clamped as an ischemia model of the nerve root and the inferior vena cava was clamped as a congestion model at the sixth costal level for 30 min using forceps transpleurally. Measurements of blood flow, partial oxygen pressure, and conduction velocity in the nerve root were repeated over a period of 1 h after release of clamping. Finally, we examined the status of intraradicular blood–nerve barrier under fluorescence and transmission electron microscope. Immediately after clamping of the inferior vena cava, the central venous pressure increased by about four times and marked extravasation of protein tracers was induced in the lumbar nerve root. Blood flow, partial oxygen pressure, and conduction velocity of the nerve root were more severely affected by aorta clamp, but this ischemia model did not show any intraradicular edema. The blood–nerve barrier in the nerve root was more easily broken by venous congestion than by arterial ishemia. In conclusion, venous congestion may be an essential factor precipitating circulatory disturbance in compressed nerve roots and inducing neurogenic intermittent claudication. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:1533–1540, 2008
Bibliography:	ark:/67375/WNG-8ZNS6RRD-R ArticleID:JOR20696 istex:3C59EB4637D423192BA8EB546D98FE527E7DD80D ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0736-0266 1554-527X
DOI:	10.1002/jor.20696