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Intestinal histopathological changes in a porcine model of pneumoperitoneum-induced intra-abdominal hypertension

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dc.contributor.authorPárraga Ros, Ester
dc.contributor.authorCorrea Martín, Laura
dc.contributor.authorSánchez‑Margallo, Francisco M.
dc.contributor.authorCandanosa‑Aranda, Irma Eugenia
dc.contributor.authorMalbrain, Manu L. N. G.
dc.contributor.authorWise, Robert
dc.contributor.authorLópez Albors, Octavio Miguel
dc.contributor.authorLatorre Reviriego, Rafael Manuel
dc.contributor.authorCastellanos, Gregorio
dc.contributor.departmentAnatomía y Anatomía Patológica Comparada
dc.date.accessioned2025-12-23T11:52:05Z
dc.date.available2025-12-23T11:52:05Z
dc.date.copyright© Springer Science+Business Media, LLC
dc.date.issued2018-05-17
dc.description.abstractBackground Low splanchnic perfusion is an immediate effect of pneumoperitoneum-induced intra-abdominal hypertension (IAH). Anatomical structure results in the intestinal mucosa being the area most sensitive to hypoperfusion. The relationship between intestinal injury and clinical parameters of tissue perfusion [abdominal perfusion pressure (APP), gastric intramucosal pH ( pHi) and lactic acid (Lc)] has not been previously studied. This study aimed to monitorize intestinal pathogenesis through sequential ileal biopsies and to measure APP, pHi, and Lc levels at different pneumoperitoneum-induced intraabdominal pressures (20, 30, and 40 mmHg) to evaluate the potential relationships between them. Materials and methods Fifty pigs were divided into four groups; a control group (C) and three experimental groups with different pneumoperitoneum-induced levels [20 mmHg (G20), 30 mmHg (G30), and 40 mmHg (G40)], that were maintained for 3 and 5 h. APP, pHi, and Lc were measured and ileal biopsies taken laparoscopically every 30 min. The mucosal damage was graded using the standardized Park’s Score and animals were classified as injured (I+) or uninjured (I−). Results Different histopathological lesions were observed in groups G20, G30, and G40 but no damage observed in group C. A 33.3% of animals in G20 and G30 were I+ after 3 h, while 93.3% were injured in G40. After 5 h, histopathological lesions were no longer seen in some animals in G20 and only 10% were I+. Conversely, in G30 I+ pigs increased to 80% while those in G40 remained at 93.3% I+. The I+ animals had significantly lower APP and pHi than those I−. Lc was the clinical parameter that showed the earliest differences, with significantly higher figures in I+ animals. Conclusions The evolution of intestinal injuries from pneumoperitoneum-induced IAH depends on the degree of IAP. These damages may be associated with decreases in APP and pHi, and increases in Lc.
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dc.format.extent14
dc.identifier.citationSurgical Endoscopy (2018) 32:3989–4002
dc.identifier.doihttps://doi.org/10.1007/s00464-018-6142-z
dc.identifier.eissn1432-2218
dc.identifier.issn0930-2794
dc.identifier.urihttp://hdl.handle.net/10201/182309
dc.languageeng
dc.publisherSpringer
dc.relationThis work was supported by one grant from Extremadura Regional Government through the Plan Regional de Investigación de Extremadura (PRI09A161 to Minimally Invasive Surgery Center Jesús Usón). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
dc.relation.publisherversionhttps://link.springer.com/article/10.1007/s00464-018-6142-z
dc.rights.accessRightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectIntestinal injury
dc.subjectHistopathological changes
dc.subjectPorcine model
dc.subjectIntra-abdominal hypertension
dc.subjectPneumoperitoneum
dc.subjectAbdominal compartment syndrome
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleIntestinal histopathological changes in a porcine model of pneumoperitoneum-induced intra-abdominal hypertension
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublicationes
relation.isAuthorOfPublication269b9699-1b31-4bb4-82ab-517084bcf737
relation.isAuthorOfPublication39ee7277-9165-4e46-adc9-72006a802990
relation.isAuthorOfPublicationd0c90149-4c92-4e44-b637-88131f331585
relation.isAuthorOfPublication.latestForDiscovery269b9699-1b31-4bb4-82ab-517084bcf737
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