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Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs

Acute kidney injury (AKI) is frequently seen in patients with hemorrhagic shock due to hypotension, tissue hypoxia, and inflammation despite adequate resuscitation. There is a lack of information concerning the alteration of renal microcirculation and perfusion during shock and resuscitation. The ai...

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Autores principales: Ergin, Bülent, van Rooij, Tom, Lima, Alex, Ince, Yasin, Specht, Patricia AC, Mik, Bert, Aksu, Ugur, Yavuz-Aksu, Berna, Kooiman, Klazina, de Jong, Nico, Ince, Can
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Netherlands 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10520149/
https://www.ncbi.nlm.nih.gov/pubmed/36745316
http://dx.doi.org/10.1007/s10877-023-00978-7
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author Ergin, Bülent
van Rooij, Tom
Lima, Alex
Ince, Yasin
Specht, Patricia AC
Mik, Bert
Aksu, Ugur
Yavuz-Aksu, Berna
Kooiman, Klazina
de Jong, Nico
Ince, Can
author_facet Ergin, Bülent
van Rooij, Tom
Lima, Alex
Ince, Yasin
Specht, Patricia AC
Mik, Bert
Aksu, Ugur
Yavuz-Aksu, Berna
Kooiman, Klazina
de Jong, Nico
Ince, Can
author_sort Ergin, Bülent
collection PubMed
description Acute kidney injury (AKI) is frequently seen in patients with hemorrhagic shock due to hypotension, tissue hypoxia, and inflammation despite adequate resuscitation. There is a lack of information concerning the alteration of renal microcirculation and perfusion during shock and resuscitation. The aim of this study was to investigate the possible role of renal microcirculatory alterations on development of renal dysfunction in a pig model of non-traumatic hemorrhagic shock (HS) induced AKI. Fully instrumented female pigs were divided into the two groups as Control (n = 6) and HS (n = 11). HS was achieved by withdrawing blood until mean arterial pressure (MAP) reached around 50 mmHg. After an hour cessation period, fluid resuscitation with balanced crystalloid was started for the duration of 1 h. The systemic and renal hemodynamics, renal microcirculatory perfusion (contrast-enhanced ultrasound (CEUS)) and the sublingual microcirculation were measured. CEUS peak enhancement was significantly increased in HS during shock, early-, and late resuscitation indicating perfusion defects in the renal cortex (p < 0.05 vs. baseline, BL) despite a stable renal blood flow (RBF) and urine output. Following normalization of systemic hemodynamics, we observed persistent hypoxia (high lactate) and high red blood cell (RBC) velocity just after initiation of resuscitation resulting in further endothelial and renal damage as shown by increased plasma sialic acid (p < 0.05 vs. BL) and NGAL levels. We also showed that total vessel density (TVD) and functional capillary density (FCD) were depleted during resuscitation (p < 0.05). In this study, we showed that the correction of systemic hemodynamic variables may not be accompanied with the improvement of renal cortical perfusion, intra-renal blood volume and renal damage following fluid resuscitation. We suggest that the measurement of renal injury biomarkers, systemic and renal microcirculation can be used for guiding to the optimization of fluid therapies.
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spelling pubmed-105201492023-09-27 Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs Ergin, Bülent van Rooij, Tom Lima, Alex Ince, Yasin Specht, Patricia AC Mik, Bert Aksu, Ugur Yavuz-Aksu, Berna Kooiman, Klazina de Jong, Nico Ince, Can J Clin Monit Comput Original Research Acute kidney injury (AKI) is frequently seen in patients with hemorrhagic shock due to hypotension, tissue hypoxia, and inflammation despite adequate resuscitation. There is a lack of information concerning the alteration of renal microcirculation and perfusion during shock and resuscitation. The aim of this study was to investigate the possible role of renal microcirculatory alterations on development of renal dysfunction in a pig model of non-traumatic hemorrhagic shock (HS) induced AKI. Fully instrumented female pigs were divided into the two groups as Control (n = 6) and HS (n = 11). HS was achieved by withdrawing blood until mean arterial pressure (MAP) reached around 50 mmHg. After an hour cessation period, fluid resuscitation with balanced crystalloid was started for the duration of 1 h. The systemic and renal hemodynamics, renal microcirculatory perfusion (contrast-enhanced ultrasound (CEUS)) and the sublingual microcirculation were measured. CEUS peak enhancement was significantly increased in HS during shock, early-, and late resuscitation indicating perfusion defects in the renal cortex (p < 0.05 vs. baseline, BL) despite a stable renal blood flow (RBF) and urine output. Following normalization of systemic hemodynamics, we observed persistent hypoxia (high lactate) and high red blood cell (RBC) velocity just after initiation of resuscitation resulting in further endothelial and renal damage as shown by increased plasma sialic acid (p < 0.05 vs. BL) and NGAL levels. We also showed that total vessel density (TVD) and functional capillary density (FCD) were depleted during resuscitation (p < 0.05). In this study, we showed that the correction of systemic hemodynamic variables may not be accompanied with the improvement of renal cortical perfusion, intra-renal blood volume and renal damage following fluid resuscitation. We suggest that the measurement of renal injury biomarkers, systemic and renal microcirculation can be used for guiding to the optimization of fluid therapies. Springer Netherlands 2023-02-06 2023 /pmc/articles/PMC10520149/ /pubmed/36745316 http://dx.doi.org/10.1007/s10877-023-00978-7 Text en © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Research
Ergin, Bülent
van Rooij, Tom
Lima, Alex
Ince, Yasin
Specht, Patricia AC
Mik, Bert
Aksu, Ugur
Yavuz-Aksu, Berna
Kooiman, Klazina
de Jong, Nico
Ince, Can
Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs
title Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs
title_full Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs
title_fullStr Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs
title_full_unstemmed Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs
title_short Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs
title_sort intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10520149/
https://www.ncbi.nlm.nih.gov/pubmed/36745316
http://dx.doi.org/10.1007/s10877-023-00978-7
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