Lung tissue apoptosis in abdominal hypertension

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dc.authorscopusid6602168584
dc.authorscopusid57057363600
dc.authorscopusid56223188000
dc.authorscopusid12042345300
dc.authorscopusid6701699128
dc.authorwosidDilek, Osman Nuri/D-7711-2018
dc.contributor.authorAkbulut, Gökhan
dc.contributor.authorYazicioglu, Murat Burç
dc.contributor.authorŞahin, Önder
dc.contributor.authorTosun, Murat
dc.contributor.authorDilek, Osman Nuri
dc.date.accessioned2022-05-11T14:36:54Z
dc.date.available2022-05-11T14:36:54Z
dc.date.issued2011
dc.departmentFakülteler, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümü, Tıbbi Patoloji Ana Bilim Dalı
dc.description.abstractObjectives The aim of this study was to evaluate lung tissue histopathologic changes and the number of apoptosis with the increase of abdominal pressure. Methods The study rats were randomly assigned into the following five groups: a sham operated group and groups 1, 2, 3 and 4, in which the intra-abdominal pressure was increased to 11, 15, 18 and 22 mmHg for 60 min, respectively. Lungs were harvested for histopathologic changes and the tissue apoptotic analysis were carried out in a blinded manner. Results All of the data showed that the number of apoptotic cells and necrosis were increased in accordance with the pressure level. However, this increase was statistically significant, especially in groups 3 and 4 (18 and 22 mmHg, respectively; p < 0.05) when compared to the sham operated rats. There were no differences observed between groups 1 and 2 (11 and 15 mmHg, respectively) and the sham operated rats. There was also no difference between groups 1 and 2. There were findings of coagulation necrosis and the number of apoptotic cells linearly increased when the abdominal pressure was increased. The cut-off value was 15 mmHg. Conclusion The available findings suggest that intra-abdominal pressure greater than 15 mmHg could irreversibly damage pulmonary cells and both coagulation necrosis parameters and the number of apoptosis increase in accordance with the pressure level.
dc.identifier.doi10.1007/s00068-010-0068-z
dc.identifier.endpage501
dc.identifier.issn1863-9933
dc.identifier.issn1863-9941
dc.identifier.issue5en_US
dc.identifier.pmid26815421
dc.identifier.scopus2-s2.0-80155189557
dc.identifier.scopusqualityQ2
dc.identifier.startpage495
dc.identifier.urihttps://doi.org/10.1007/s00068-010-0068-z
dc.identifier.urihttps://hdl.handle.net/20.500.11776/8467
dc.identifier.volume37
dc.identifier.wosWOS:000296292000009
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorŞahin, Önder
dc.language.isoen
dc.publisherSpringer Heidelberg
dc.relation.ispartofEuropean Journal of Trauma and Emergency Surgery
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectOpen abdomen
dc.subjectAbdominal
dc.subjectExperimental trauma surgery
dc.subjectGeneral trauma
dc.subjectThoracic
dc.subjectThoracic and abdominal
dc.subjectIncreased Intraabdominal Pressure
dc.subjectRespiratory-Distress-Syndrome
dc.subjectCompartment Syndrome
dc.subjectInternational-Conference
dc.subjectPulmonary
dc.subjectExperts
dc.titleLung tissue apoptosis in abdominal hypertension
dc.typeArticle

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