Protective effect of posterior cerebral circulation on carotid body ischemia

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dc.contributor.authorAydin, MD
dc.contributor.authorÖzkan, U
dc.contributor.authorGündogdu, C
dc.contributor.authorÖnder, A
dc.date.accessioned2024-04-24T16:01:57Z
dc.date.available2024-04-24T16:01:57Z
dc.date.issued2002
dc.departmentDicle Üniversitesien_US
dc.description.abstractBackground and Purpose. Carotid Bodies (CB) are fed mainly by External Carotid Artery (ECA) and rarely by Internal Carotid Artery (ICA). We aimed to investigate the effect of Bilateral Common Carotid Artery ligation and BCCAL plus bilateral external carotid artery ligation on CB. Methods. This study has been conducted on 30 hybrid male rabbits. Normal CB analyses were made in six of these animals and others divided into two groups. BCCAL has been applied to the 1st group, and the 2nd group has undergone bilateral ECA ligation in addition to BCCAL. After sacrificing the animals, both sides CB were histopathologically observed. Normal and ischemic cells were counted. Findings. Bilateral Common Carotid Artery ligation did not cause total atrophy in CB. Partial reversible atrophy of CB was seen in group 1, but that atrophy was found to be irreversible and all animals died within one week after ligation in group II. Interpretation. Retrograde blood flow mechanisms and collateral circulation impede the oligemic CB atrophy after BCCAL. But bilateral ECA ligation, in addition to BCCAL, causes both sides irreversible CB atrophy and death of animals within one week of ligation. Abstract. The CB are parasympathetic paraganglia. They are chemoreceptors and located at the bifurcation zone of common carotid arteries. They are fed mainly by ECA or by its branches and rarely by ICA. As a consequence of this, BCCAL and/or ligation of external branches of common carotid artery may lead to an ischemic impairment of CB. In order to analyse the effect of carotid stenosis on CB, CB were directly examined in 6 of 30 hybrid rabbits. BCCAL was applied to twelve rabbits (group 1) with ligation of both ECA in addition to BCCAL were made to the others (group II). Animals were followed up four months in group I; but all of the animals in group II died within one week. From both sides the CB were taken including the carotid bifurcation and histopathological changes were evaluated. As a result, it has been observed that incomplete ischemic lesions have developed in the CB because of retrograde blood flow from posterior circulation to the ECA providing blood for the CB. But in the second group these changes were irreversible and on both sides CB complete atrophy developed in those whose ECA were also ligated bilaterally.en_US
dc.identifier.doi10.1007/s007010200051
dc.identifier.endpage372en_US
dc.identifier.issn0001-6268
dc.identifier.issue4en_US
dc.identifier.pmid12021884
dc.identifier.scopus2-s2.0-0036255011
dc.identifier.scopusqualityQ1
dc.identifier.startpage369en_US
dc.identifier.urihttps://doi.org/10.1007/s007010200051
dc.identifier.urihttps://hdl.handle.net/11468/14526
dc.identifier.volume144en_US
dc.identifier.wosWOS:000175187200009
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherSpringer-Verlag Wienen_US
dc.relation.ispartofActa Neurochirurgica
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCarotid Body Ischemiaen_US
dc.subjectCommon Carotid Occlusionen_US
dc.subjectAtrophyen_US
dc.titleProtective effect of posterior cerebral circulation on carotid body ischemiaen_US
dc.titleProtective effect of posterior cerebral circulation on carotid body ischemia
dc.typeArticleen_US

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