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Local cerebral blood flow during and after bilateral carotid artery occlusion in unanesthetized gerbils
Using [14C]iodoantipyrine autoradiography, we measured regional cerebral blood flow in unanesthetized gerbils subjected to 2 (n = 5) or 30 (n = 6) minutes of bilateral carotid artery occlusion or 5 (n = 6), 30 (n = 6), or 120 (n = 5) minutes of reflow after 30 minutes of occlusion. Blood pressure, r...
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Published in: | Stroke (1970) 1990-06, Vol.21 (6), p.901-907 |
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creator | NADASY, G. L GREENBERG, J. H REIVICH, M KOVACH, A. G. B |
description | Using [14C]iodoantipyrine autoradiography, we measured regional cerebral blood flow in unanesthetized gerbils subjected to 2 (n = 5) or 30 (n = 6) minutes of bilateral carotid artery occlusion or 5 (n = 6), 30 (n = 6), or 120 (n = 5) minutes of reflow after 30 minutes of occlusion. Blood pressure, respiratory rate, and blood gases were recorded, and these and other gerbils were evaluated with periodic neurologic examinations. Blood flow to structures above the level of the diencephalon ceased almost totally during occlusion. The lateral thalamus, the rostral three quarters of the hypothalamus, and the superior colliculi were also markedly ischemic. Blood flow to the brainstem and cerebellum was only slightly affected. After release of the occlusion, blood flow was restored in some of the affected areas but to levels somewhat below that in eight sham-operated gerbils. In several areas, principally column-shaped areas in the cortex as well as patchy areas in other structures, blood flow did not recover. This inhomogeneous blood flow distribution lasted at least 30 minutes after release of the occlusion. Thereafter, the inhomogeneity slowly disappeared in such a manner that blood flow to originally well reperfused areas appeared to decrease while that to poorly reperfused areas increased. During reflow, blood flow in the brainstem and cerebellum slowly and continuously decreased. We show that there is an early no-reflow phenomenon that is inhomogeneous and appears to be of vascular origin and lasts approximately 30 minutes after release of the occlusion. |
doi_str_mv | 10.1161/01.STR.21.6.901 |
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L ; GREENBERG, J. H ; REIVICH, M ; KOVACH, A. G. B</creator><creatorcontrib>NADASY, G. L ; GREENBERG, J. H ; REIVICH, M ; KOVACH, A. G. B</creatorcontrib><description>Using [14C]iodoantipyrine autoradiography, we measured regional cerebral blood flow in unanesthetized gerbils subjected to 2 (n = 5) or 30 (n = 6) minutes of bilateral carotid artery occlusion or 5 (n = 6), 30 (n = 6), or 120 (n = 5) minutes of reflow after 30 minutes of occlusion. Blood pressure, respiratory rate, and blood gases were recorded, and these and other gerbils were evaluated with periodic neurologic examinations. Blood flow to structures above the level of the diencephalon ceased almost totally during occlusion. The lateral thalamus, the rostral three quarters of the hypothalamus, and the superior colliculi were also markedly ischemic. Blood flow to the brainstem and cerebellum was only slightly affected. After release of the occlusion, blood flow was restored in some of the affected areas but to levels somewhat below that in eight sham-operated gerbils. In several areas, principally column-shaped areas in the cortex as well as patchy areas in other structures, blood flow did not recover. This inhomogeneous blood flow distribution lasted at least 30 minutes after release of the occlusion. Thereafter, the inhomogeneity slowly disappeared in such a manner that blood flow to originally well reperfused areas appeared to decrease while that to poorly reperfused areas increased. During reflow, blood flow in the brainstem and cerebellum slowly and continuously decreased. 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H</creatorcontrib><creatorcontrib>REIVICH, M</creatorcontrib><creatorcontrib>KOVACH, A. G. B</creatorcontrib><title>Local cerebral blood flow during and after bilateral carotid artery occlusion in unanesthetized gerbils</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Using [14C]iodoantipyrine autoradiography, we measured regional cerebral blood flow in unanesthetized gerbils subjected to 2 (n = 5) or 30 (n = 6) minutes of bilateral carotid artery occlusion or 5 (n = 6), 30 (n = 6), or 120 (n = 5) minutes of reflow after 30 minutes of occlusion. Blood pressure, respiratory rate, and blood gases were recorded, and these and other gerbils were evaluated with periodic neurologic examinations. Blood flow to structures above the level of the diencephalon ceased almost totally during occlusion. The lateral thalamus, the rostral three quarters of the hypothalamus, and the superior colliculi were also markedly ischemic. Blood flow to the brainstem and cerebellum was only slightly affected. After release of the occlusion, blood flow was restored in some of the affected areas but to levels somewhat below that in eight sham-operated gerbils. In several areas, principally column-shaped areas in the cortex as well as patchy areas in other structures, blood flow did not recover. This inhomogeneous blood flow distribution lasted at least 30 minutes after release of the occlusion. Thereafter, the inhomogeneity slowly disappeared in such a manner that blood flow to originally well reperfused areas appeared to decrease while that to poorly reperfused areas increased. During reflow, blood flow in the brainstem and cerebellum slowly and continuously decreased. We show that there is an early no-reflow phenomenon that is inhomogeneous and appears to be of vascular origin and lasts approximately 30 minutes after release of the occlusion.</description><subject>Animals</subject><subject>Arterial Occlusive Diseases - physiopathology</subject><subject>Autoradiography</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Brain - blood supply</subject><subject>Carotid Artery Diseases - physiopathology</subject><subject>Cerebrovascular Circulation</subject><subject>Gerbillinae</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system involvement in other diseases. Miscellaneous</subject><subject>Neurologic Examination</subject><subject>Neurology</subject><subject>Perfusion</subject><subject>Seizures - physiopathology</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><recordid>eNpFkMtLxDAQxoMouj7OnoRc9NZuJk0fOYr4ggVB13NI08ka6TaatIj-9WbZRU8z8803H8OPkHNgOUAFcwb5y_I555BXuWSwR2ZQcpGJijf7ZMZYITMupDwixzG-M8Z40ZSH5JAXQpZSzMhq4Y3uqcGAbUhN23vfUdv7L9pNwQ0rqoeOajtioK3rdaobuw5-dEkPaf6m3ph-is4P1A10GvSAcXzD0f1gR1cY0l08JQdW9xHPdvWEvN7dLm8essXT_ePN9SIzhWzGTCK0WFisqgJqYaWwmEZRt9xCU3ZYQmd1A6VkTSOMBLR2o9oSNG-htcUJudrmfgT_OaU_1NpFg32fnvJTVLVsgNelTMb51miCjzGgVR_BrXX4VsDUBq1ioBJaxUFVKqFNFxe76KldY_fn37FM-8vdXsfE1AY9GBf_Y2XFa1bL4hf55YPK</recordid><startdate>19900601</startdate><enddate>19900601</enddate><creator>NADASY, G. L</creator><creator>GREENBERG, J. H</creator><creator>REIVICH, M</creator><creator>KOVACH, A. G. 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B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-9e1be3fe663174f94fee3f47b2f185de51dfa81590884c91eff5de5f51a2b1bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Animals</topic><topic>Arterial Occlusive Diseases - physiopathology</topic><topic>Autoradiography</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Brain - blood supply</topic><topic>Carotid Artery Diseases - physiopathology</topic><topic>Cerebrovascular Circulation</topic><topic>Gerbillinae</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system involvement in other diseases. Miscellaneous</topic><topic>Neurologic Examination</topic><topic>Neurology</topic><topic>Perfusion</topic><topic>Seizures - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NADASY, G. L</creatorcontrib><creatorcontrib>GREENBERG, J. H</creatorcontrib><creatorcontrib>REIVICH, M</creatorcontrib><creatorcontrib>KOVACH, A. G. B</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NADASY, G. L</au><au>GREENBERG, J. H</au><au>REIVICH, M</au><au>KOVACH, A. G. B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Local cerebral blood flow during and after bilateral carotid artery occlusion in unanesthetized gerbils</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>1990-06-01</date><risdate>1990</risdate><volume>21</volume><issue>6</issue><spage>901</spage><epage>907</epage><pages>901-907</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Using [14C]iodoantipyrine autoradiography, we measured regional cerebral blood flow in unanesthetized gerbils subjected to 2 (n = 5) or 30 (n = 6) minutes of bilateral carotid artery occlusion or 5 (n = 6), 30 (n = 6), or 120 (n = 5) minutes of reflow after 30 minutes of occlusion. Blood pressure, respiratory rate, and blood gases were recorded, and these and other gerbils were evaluated with periodic neurologic examinations. Blood flow to structures above the level of the diencephalon ceased almost totally during occlusion. The lateral thalamus, the rostral three quarters of the hypothalamus, and the superior colliculi were also markedly ischemic. Blood flow to the brainstem and cerebellum was only slightly affected. After release of the occlusion, blood flow was restored in some of the affected areas but to levels somewhat below that in eight sham-operated gerbils. In several areas, principally column-shaped areas in the cortex as well as patchy areas in other structures, blood flow did not recover. This inhomogeneous blood flow distribution lasted at least 30 minutes after release of the occlusion. Thereafter, the inhomogeneity slowly disappeared in such a manner that blood flow to originally well reperfused areas appeared to decrease while that to poorly reperfused areas increased. During reflow, blood flow in the brainstem and cerebellum slowly and continuously decreased. We show that there is an early no-reflow phenomenon that is inhomogeneous and appears to be of vascular origin and lasts approximately 30 minutes after release of the occlusion.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>2349594</pmid><doi>10.1161/01.STR.21.6.901</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Arterial Occlusive Diseases - physiopathology Autoradiography Biological and medical sciences Blood Pressure Brain - blood supply Carotid Artery Diseases - physiopathology Cerebrovascular Circulation Gerbillinae Male Medical sciences Nervous system involvement in other diseases. Miscellaneous Neurologic Examination Neurology Perfusion Seizures - physiopathology |
title | Local cerebral blood flow during and after bilateral carotid artery occlusion in unanesthetized gerbils |
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