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   <subfield code="a">Endothelial-cell injury of the basilar artery caused by ethanol infusion in dogs</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[H. Kobayashi, H. Ide, M. Kabuto, Y. Handa, T. Kubota]</subfield>
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   <subfield code="a">Summary: This study in mongrel dogs was designed to observe the effects of ethanol on both endothelial cells of the basilar artery and brain function. By use of sterile surgical technique, a super-selective catheter was placed in the proximal portion of the basilar artery in the dogs. Five dogs received 3 ml of 25% ethanol and 5 dogs received 3 ml of 50% of ethanol through the catheter over 2 minutes. The remaining 5 dogs received 3 ml of saline as a control. Auditory brain stem response (ABR) was monitored for 2 hours after ethanol infusion, and then perfusion-fixation was performed from the heart with 4% paraformaldehyde. The basilar artery was observed with scanning electron microscopy after routine procedures. The endothelial cells were intact in the control group. The 50% group showed a higher level of injury to the endothelium as well as a higher degree of platelet adhesion and fibrin clot formation compared with the 25% group. The extensive endothelial-cell damage subsequently caused thrombus formation. The ABR disappeared immediately after ethanol infusion in both ethanol groups, and recovered gradually in the 25% group, but did not re-appear during the time course of 2 hours in the 50% group. The ethanol less than 25% in concentration near the endothelium is considered to be safe as a transcatheter embolic agent with the attention to the central toxicity.</subfield>
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   <subfield code="a">Springer-Verlag, 1996</subfield>
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   <subfield code="a">Auditory brain stem response</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">basilar artery</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">ethanol</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">endothelial cell damage</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Kobayashi</subfield>
   <subfield code="D">H.</subfield>
   <subfield code="u">Department of Neurosurgery, Fukui Medical School, Fukui, Japan</subfield>
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   <subfield code="a">Ide</subfield>
   <subfield code="D">H.</subfield>
   <subfield code="u">Department of Neurosurgery, Fukui Medical School, Fukui, Japan</subfield>
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   <subfield code="a">Kabuto</subfield>
   <subfield code="D">M.</subfield>
   <subfield code="u">Department of Neurosurgery, Fukui Medical School, Fukui, Japan</subfield>
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   <subfield code="a">Handa</subfield>
   <subfield code="D">Y.</subfield>
   <subfield code="u">Department of Neurosurgery, Fukui Medical School, Fukui, Japan</subfield>
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   <subfield code="a">Kubota</subfield>
   <subfield code="D">T.</subfield>
   <subfield code="u">Department of Neurosurgery, Fukui Medical School, Fukui, Japan</subfield>
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   <subfield code="t">Acta Neurochirurgica</subfield>
   <subfield code="d">Springer-Verlag</subfield>
   <subfield code="g">138/1(1996-01-01), 84-89</subfield>
   <subfield code="x">0001-6268</subfield>
   <subfield code="q">138:1&lt;84</subfield>
   <subfield code="1">1996</subfield>
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