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  • 1
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    Partial Deletion of Tie2 Affects Microvascular Endothelial Responses to Critical Illness in A Vascular Bed and Organ-Specific Way
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Shock Vol. 51, No. 6 ( 2019-06), p. 757-769
    Details
    In: Shock, Ovid Technologies (Wolters Kluwer Health), Vol. 51, No. 6 ( 2019-06), p. 757-769
    Abstract: Tyrosine kinase receptor (Tie2) is mainly expressed by endothelial cells. In animal models mimicking critical illness, Tie2 levels in organs are temporarily reduced. Functional consequences of these reduced Tie2 levels on microvascular endothelial behavior are unknown. We investigated the effect of partial deletion of Tie2 on the inflammatory status of endothelial cells in different organs. Newly generated heterozygous Tie2 knockout mice (exon 9 deletion, ΔE9/Tie2 +/− ) exhibiting 50% reduction in Tie2 mRNA and protein, and wild-type littermate controls (Tie2 +/+ ), were subjected to hemorrhagic shock and resuscitation (HS + R), or challenged with i.p. lipopolysaccharide (LPS). Kidney, liver, lung, heart, brain, and intestine were analyzed for mRNA levels of adhesion molecules E-selectin, vascular cell adhesion molecule 1 (VCAM-1), and intercellular cell adhesion molecule 1 (ICAM-1), and CD45. Exposure to HS + R did not result in different expression responses of these molecules between organs from Tie2 +/− or Tie2 +/+ mice and sham-operated mice. In contrast, the LPS-induced mRNA expression levels of E-selectin, VCAM-1, and ICAM-1, and CD45 in organs were attenuated in Tie2 +/− mice when compared with Tie2 +/+ mice in kidney and liver, but not in the other organs studied. Furthermore, reduced expression of E-selectin and VCAM-1 protein, and reduced influx of CD45 + cells upon LPS exposure, was visible in a microvascular bed-specific pattern in kidney and liver of Tie2 +/− mice compared with controls. In contrast to the hypothesis that a disbalance in the Ang/Tie2 system leads to increased microvascular inflammation, heterozygous deletion of Tie2 is associated with an organ-restricted, microvascular bed-specific attenuation of endothelial inflammatory response to LPS.
    Type of Medium: Online Resource
    ISSN: 1073-2322 , 1540-0514
    URL: Article
    DOI: 10.1097/SHK.0000000000001226
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2011863-6
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  • 2
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    Sepsis is associated with mitochondrial DNA damage and a reduced mitochondrial mass in the kidney of patients with sepsis-AKI
    Springer Science and Business Media LLC ; 2021
    In:  Critical Care Vol. 25, No. 1 ( 2021-12)
    Details
    In: Critical Care, Springer Science and Business Media LLC, Vol. 25, No. 1 ( 2021-12)
    Abstract: Sepsis is a life-threatening condition accompanied by organ dysfunction subsequent to a dysregulated host response to infection. Up to 60% of patients with sepsis develop acute kidney injury (AKI), which is associated with a poor clinical outcome. The pathophysiology of sepsis-associated AKI (sepsis-AKI) remains incompletely understood, but mitochondria have emerged as key players in the pathogenesis. Therefore, our aim was to identify mitochondrial damage in patients with sepsis-AKI. Methods We conducted a clinical laboratory study using “warm” postmortem biopsies from sepsis-associated AKI patients from a university teaching hospital. Biopsies were taken from adult patients ( n  = 14) who died of sepsis with AKI at the intensive care unit (ICU) and control patients ( n  = 12) undergoing tumor nephrectomy. To define the mechanisms of the mitochondrial contribution to the pathogenesis of sepsis-AKI, we explored mRNA and DNA expression of mitochondrial quality mechanism pathways, DNA oxidation and mitochondrial DNA (mtDNA) integrity in renal biopsies from sepsis-AKI patients and control subjects. Next, we induced human umbilical vein endothelial cells (HUVECs) with lipopolysaccharide (LPS) for 48 h to mimic sepsis and validate our results in vitro. Results Compared to control subjects, sepsis-AKI patients had upregulated mRNA expression of oxidative damage markers, excess mitochondrial DNA damage and lower mitochondrial mass. Sepsis-AKI patients had lower mRNA expression of mitochondrial quality markers TFAM , PINK1 and PARKIN , but not of MFN2 and DRP1 . Oxidative DNA damage was present in the cytosol of tubular epithelial cells in the kidney of sepsis-AKI patients, whereas it was almost absent in biopsies from control subjects. Oxidative DNA damage co-localized with both the nuclei and mitochondria. Accordingly, HUVECs induced with LPS for 48 h showed an increased mnSOD expression, a decreased TFAM expression and higher mtDNA damage levels. Conclusion Sepsis-AKI induces mitochondrial DNA damage in the human kidney, without upregulation of mitochondrial quality control mechanisms, which likely resulted in a reduction in mitochondrial mass.
    Type of Medium: Online Resource
    ISSN: 1364-8535
    URL: Article
    DOI: 10.1186/s13054-020-03424-1
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2051256-9
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  • 3
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    Intracellular RIG-I Signaling Regulates TLR4-Independent Endothelial Inflammatory Responses to Endotoxin
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 196, No. 11 ( 2016-06-01), p. 4681-4691
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 196, No. 11 ( 2016-06-01), p. 4681-4691
    Abstract: Sepsis is a systemic inflammatory response to infections associated with organ failure that is the most frequent cause of death in hospitalized patients. Exaggerated endothelial activation, altered blood flow, vascular leakage, and other disturbances synergistically contribute to sepsis-induced organ failure. The underlying signaling events associated with endothelial proinflammatory activation are not well understood, yet they likely consist of molecular pathways that act in an endothelium-specific manner. We found that LPS, a critical factor in the pathogenesis of sepsis, is internalized by endothelial cells, leading to intracellular signaling without the need for priming as found recently in immune cells. By identifying a novel role for retinoic acid–inducible gene-I (RIG-I) as a central regulator of endothelial activation functioning independent of TLR4, we provide evidence that the current paradigm of TLR4 solely being responsible for LPS-mediated endothelial responses is incomplete. RIG-I, as well as the adaptor protein mitochondrial antiviral signaling protein, regulates NF-κB–mediated induction of adhesion molecules and proinflammatory cytokine expression in response to LPS. Our findings provide essential new insights into the proinflammatory signaling pathways in endothelial cells and suggest that combined endothelial-specific inhibition of RIG-I and TLR4 will provide protection from aberrant endothelial responses associated with sepsis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1501819
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 4
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    Preservation of renal endothelial integrity and reduction of renal edema by aprotinin does not preserve renal perfusion and function following experimental cardiopulmonary bypass
    Springer Science and Business Media LLC ; 2021
    In:  Intensive Care Medicine Experimental Vol. 9, No. 1 ( 2021-12)
    Details
    In: Intensive Care Medicine Experimental, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2021-12)
    Abstract: Acute kidney injury is a severe complication following cardiopulmonary bypass (CPB) and is associated with capillary leakage and microcirculatory perfusion disturbances. CPB-induced thrombin release results in capillary hyperpermeability via activation of protease-activated receptor 1 (PAR1). We investigated whether aprotinin, which is thought to prevent thrombin from activating PAR1, preserves renal endothelial structure, reduces renal edema and preserves renal perfusion and reduces renal injury following CPB. Methods Rats were subjected to CPB after treatment with 33.000 KIU/kg aprotinin ( n  = 15) or PBS ( n  = 15) as control. A secondary dose of 33.000 KIU/kg aprotinin was given 60 min after initiation of CPB. Cremaster and renal microcirculatory perfusion were assessed using intravital microscopy and contrast echography before CPB and 10 and 60 min after weaning from CPB. Renal edema was determined by wet/dry weight ratio and renal endothelial structure by electron microscopy. Renal PAR1 gene and protein expression and markers of renal injury were determined. Results CPB reduced cremaster microcirculatory perfusion by 2.5-fold (15 (10–16) to 6 (2–10) perfused microvessels, p   〈  0.0001) and renal perfusion by 1.6-fold (202 (67–599) to 129 (31–292) au/sec, p  = 0.03) in control animals. Both did not restore 60 min post-CPB. This was paralleled by increased plasma creatinine ( p   〈  0.01), neutrophil gelatinase-associated lipocalin (NGAL; p  = 0.003) and kidney injury molecule-1 (KIM-1; p   〈  0.01). Aprotinin treatment preserved cremaster microcirculatory perfusion following CPB (12 (7–15) vs. 6 (2–10) perfused microvessels, p  = 0.002), but not renal perfusion (96 (35–313) vs. 129 (31–292) au/s, p   〉  0.9) compared to untreated rats. Aprotinin treatment reduced endothelial gap formation (0.5 ± 0.5 vs. 3.1 ± 1.4 gaps, p   〈  0.0001), kidney wet/dry weight ratio (4.6 ± 0.2 vs. 4.4 ± 0.2, p  = 0.046), and fluid requirements (3.9 ± 3.3 vs. 7.5 ± 3.0 ml, p  = 0.006) compared to untreated rats. In addition, aprotinin treatment reduced tubulointerstitial neutrophil influx by 1.7-fold compared to untreated rats (30.7 ± 22.1 vs. 53.2 ± 17.2 neutrophil influx/section, p  = 0.009). No differences were observed in renal PAR1 expression and plasma creatinine, NGAL or KIM-1 between groups. Conclusions Aprotinin did not improve renal perfusion nor reduce renal injury during the first hour following experimental CPB despite preservation of renal endothelial integrity and reduction of renal edema.
    Type of Medium: Online Resource
    ISSN: 2197-425X
    URL: Article
    DOI: 10.1186/s40635-021-00393-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2740385-3
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  • 5
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    PRESERVATION OF RENAL ENDOTHELIAL INTEGRITY AND REDUCITON OF RENAL EDEMA BY APROTININ DOES NOT PRESERVE RENAL PERFUSION AND FUNCTION FOLLOWING EXPERIMENTAL CARDIOPULMONARY BYPASS
    Elsevier BV ; 2021
    In:  Journal of Cardiothoracic and Vascular Anesthesia Vol. 35 ( 2021-10), p. S10-S11
    Details
    In: Journal of Cardiothoracic and Vascular Anesthesia, Elsevier BV, Vol. 35 ( 2021-10), p. S10-S11
    Type of Medium: Online Resource
    ISSN: 1053-0770
    URL: Article
    DOI: 10.1053/j.jvca.2021.08.055
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2043630-0
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  • 6
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    Vasculotide, an Angiopoietin-1 Mimetic, Restores Microcirculatory Perfusion and Microvascular Leakage and Decreases Fluid Resuscitation Requirements in Hemorrhagic Shock
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Anesthesiology Vol. 128, No. 2 ( 2018-02-01), p. 361-374
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 128, No. 2 ( 2018-02-01), p. 361-374
    Abstract: Microcirculatory dysfunction is associated with multiple organ failure and unfavorable patient outcome. We investigated whether therapeutically targeting the endothelial angiopoietin/Tie2 system preserves microvascular integrity during hemorrhagic shock. Methods Rats were treated with the angiopoietin-1 mimetic vasculotide and subjected to hemorrhagic shock and fluid resuscitation. Microcirculatory perfusion and leakage were assessed with intravital microscopy (n = 7 per group) and Evans blue dye extravasation (n = 8 per group), respectively. The angiopoietin/Tie2 system was studied at protein and RNA level in plasma, kidneys, and lungs. Results Hemorrhagic shock significantly reduced continuously perfused capillaries (7 ± 2 vs. 11 ± 2) and increased nonperfused vessels (9 ± 3 vs. 5 ± 2) during hemorrhagic shock, which could not be restored by fluid resuscitation. Hemorrhagic shock increased circulating angiopoietin-2 and soluble Tie2 significantly, which associated with microcirculatory perfusion disturbances. Hemorrhagic shock significantly decreased Tie2 gene expression in kidneys and lungs and induced microvascular leakage in kidneys (19.7 ± 11.3 vs. 5.2 ± 3.0 µg/g) and lungs (16.1 ± 7.0 vs. 8.6 ± 2.7 µg/g). Vasculotide had no effect on hemodynamics and microcirculatory perfusion during hemorrhagic shock but restored microcirculatory perfusion during fluid resuscitation. Interestingly, vasculotide attenuated microvascular leakage in lungs (10.1 ± 3.3 µg/g) and significantly reduced the required amount of volume supplementation (1.3 ± 1.4 vs. 2.8 ± 1.5 ml). Furthermore, vasculotide posttreatment was also able to restore microcirculatory perfusion during fluid resuscitation. Conclusions Targeting Tie2 restored microvascular leakage and microcirculatory perfusion and reduced fluid resuscitation requirements in an experimental model of hemorrhagic shock. Therefore, the angiopoietin/Tie2 system seems to be a promising target in restoring microvascular integrity and may reduce organ failure during hemorrhagic shock.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/ALN.0000000000001907
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2016092-6
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  • 7
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    Circulating adipokine levels and COVID-19 severity in hospitalized patients
    Springer Science and Business Media LLC ; 2023
    In:  International Journal of Obesity Vol. 47, No. 2 ( 2023-02), p. 126-137
    Details
    In: International Journal of Obesity, Springer Science and Business Media LLC, Vol. 47, No. 2 ( 2023-02), p. 126-137
    Abstract: Obesity is a risk factor for adverse outcomes in COVID-19, potentially driven by chronic inflammatory state due to dysregulated secretion of adipokines and cytokines. We investigated the association between plasma adipokines and COVID-19 severity, systemic inflammation, clinical parameters, and outcome of COVID-19 patients. Methods In this multi-centre prospective cross-sectional study, we collected blood samples and clinical data from COVID-19 patients. The severity of COVID-19 was classified as mild (no hospital admission), severe (ward admission), and critical (ICU admission). ICU non-COVID-19 patients were also included and plasma from healthy age, sex, and BMI-matched individuals obtained from Lifelines. Multi-analyte profiling of plasma adipokines (Leptin, Adiponectin, Resistin, Visfatin) and inflammatory markers (IL-6, TNFα, IL-10) were determined using Luminex multiplex assays. Results Between March and December 2020, 260 SARS-CoV-2 infected individuals (age: 65 [56–74] BMI 27.0 [24.4–30.6] ) were included: 30 mild, 159 severe, and 71 critical patients. Circulating leptin levels were reduced in critically ill patients with a high BMI yet this decrease was absent in patients that were administered dexamethasone. Visfatin levels were higher in critical COVID-19 patients compared to non-COVID-ICU, mild and severe patients (4.7 vs 3.4, 3.0, and 3.72 ng/mL respectively, p   〈  0.05). Lower Adiponectin levels, but higher Resistin levels were found in severe and critical patients, compared to those that did not require hospitalization (3.65, 2.7 vs 7.9 µg/mL, p   〈  0.001, and 18.2, 22.0 vs 11.0 ng/mL p   〈  0.001). Conclusion Circulating adipokine levels are associated with COVID-19 hospitalization, i.e., the need for oxygen support (general ward), or the need for mechanical ventilation and other organ support in the ICU, but not mortality.
    Type of Medium: Online Resource
    ISSN: 0307-0565 , 1476-5497
    URL: Article
    DOI: 10.1038/s41366-022-01246-5
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2101927-7
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  • 8
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    Acute Kidney Injury is Associated with Lowered Plasma-Free Thiol Levels
    MDPI AG ; 2020
    In:  Antioxidants Vol. 9, No. 11 ( 2020-11-16), p. 1135-
    Details
    In: Antioxidants, MDPI AG, Vol. 9, No. 11 ( 2020-11-16), p. 1135-
    Abstract: Acute kidney injury (AKI) is associated with the abrupt loss of kidney function. Oxidative stress plays an important role in the pathophysiology of AKI. Free thiols (R-SH) are crucial components of the extracellular antioxidant machinery and reliably reflect systemic oxidative stress. Lower levels of thiols represent higher levels of oxidative stress. In this preliminary study, we hypothesized that plasma-free thiols are associated with AKI upon admission to the intensive care unit (ICU). In this study, 301 critically ill patients were included. Plasma samples were taken upon admission, and albumin-adjusted plasma-free thiols were determined. Albumin-adjusted plasma-free thiols were lower in patients with AKI (n = 43, median (interquartile range) 7.28 µmol/g (3.52, 8.95)) compared to patients without AKI (8.50 μmol/g (5.82, 11.28); p 〈 0.05) upon admission to the ICU. Higher age (B = −0.72), higher levels of neutrophil gelatinase-associated lipocalin (B = −0.002), creatinine (B = −0.01) and lower serum albumin (B = 0.47) were associated with lower free thiol levels. Further, albumin-adjusted free thiol levels were significantly reduced in patients with sepsis (8.30 (5.52–10.64) µmol/g) compared to patients without sepsis (6.95 (3.72–8.92) µmol/g; p 〈 0.05). Together, albumin-adjusted plasma-free thiols were significantly reduced in patients with AKI and patients with sepsis compared with patients without AKI and sepsis.
    Type of Medium: Online Resource
    ISSN: 2076-3921
    URL: Article
    DOI: 10.3390/antiox9111135
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2704216-9
    SSG: 15,3
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  • 9
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    Immediate sonography and intervention in blunt chest trauma: A case report
    SAGE Publications ; 2023
    In:  SAGE Open Medical Case Reports Vol. 11 ( 2023-01)
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    In: SAGE Open Medical Case Reports, SAGE Publications, Vol. 11 ( 2023-01)
    Abstract: Cardiac tamponade is a leading cause of death in blunt thoracic trauma. Ultrasound improved the recognition of cardiac tamponade and therefore has a vital role in acute critical situations in the Emergency Department and in the Intensive Care Unit. Besides recognition of cardiac tamponade, treatment protocols are important. In trauma patients with hemodynamic stable cardiac tamponade, time should be taken for a proper workup for an explorative sternotomy. In hemodynamic unstable trauma patients, the pericardium should be drained, and fluid resuscitation should be performed followed by emergency sternotomy. In this case report we describe a blunt thoracic trauma victim, a 28-year-old male patient without any medical history. He suffered from the unique combination of a tear in the left atrial appendage and a papillary muscle rupture of the right ventricle because of blunt thoracic trauma. Transthoracic echocardiography revealed massive pericardial effusion with diastolic collapse of the right ventricle in our patient. Due to his hemodynamic situation, the patient was brought into the OR for immediate sternotomy and cardiac repair. The patient made a full recovery, was discharged home, and is back to work. This case report emphasizes the relevance of early recognition and treatment of cardiac tamponade in blunt thoracic trauma victims and suggests a multidisciplinary management strategy.
    Type of Medium: Online Resource
    ISSN: 2050-313X , 2050-313X
    URL: Article
    DOI: 10.1177/2050313X231204195
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2023
    detail.hit.zdb_id: 2736953-5
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  • 10
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    The effect of targeting Tie2 on hemorrhagic shock-induced renal perfusion disturbances in rats
    Springer Science and Business Media LLC ; 2021
    In:  Intensive Care Medicine Experimental Vol. 9, No. 1 ( 2021-05-17)
    Details
    In: Intensive Care Medicine Experimental, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2021-05-17)
    Abstract: Hemorrhagic shock is associated with acute kidney injury and increased mortality. Targeting the endothelial angiopoietin/Tie2 system, which regulates endothelial permeability, previously reduced hemorrhagic shock-induced vascular leakage. We hypothesized that as a consequence of vascular leakage, renal perfusion and function is impaired and that activating Tie2 restores renal perfusion and function. Methods Rats underwent 1 h of hemorrhagic shock and were treated with either vasculotide or PBS as control, followed by fluid resuscitation for 4 h. Microcirculatory perfusion was measured in the renal cortex and cremaster muscle using contrast echography and intravital microscopy, respectively. Changes in the angiopoietin/Tie2 system and renal injury markers were measured in plasma and on protein and mRNA level in renal tissue. Renal edema formation was determined by wet/dry weight ratios and renal structure by histological analysis. Results Hemorrhagic shock significantly decreased renal perfusion (240 ± 138 to 51 ± 40, p   〈  0.0001) and cremaster perfusion (12 ± 2 to 5 ± 2 perfused vessels, p   〈  0.0001) compared to baseline values. Fluid resuscitation partially restored both perfusion parameters, but both remained below baseline values (renal perfusion 120 ± 58, p  = 0.08, cremaster perfusion 7 ± 2 perfused vessels, p   〈  0.0001 compared to baseline). Hemorrhagic shock increased circulating angiopoietin-1 ( p   〈  0.0001), angiopoietin-2 ( p   〈  0.0001) and soluble Tie2 ( p  = 0.05), of which angiopoietin-2 elevation was associated with renal edema formation (r = 0.81, p   〈  0.0001). Hemorrhagic shock induced renal injury, as assessed by increased levels of plasma neutrophil gelatinase-associated lipocalin (NGAL: p   〈  0.05), kidney injury marker-1 (KIM-1; p   〈  0.01) and creatinine ( p   〈  0.05). Vasculotide did not improve renal perfusion ( p   〉  0.9 at all time points) or reduce renal injury (NGAL p  = 0.26, KIM-1 p  = 0.78, creatinine p   〉  0.9, renal edema p  = 0.08), but temporarily improved cremaster perfusion at 3 h following start of fluid resuscitation compared to untreated rats (resuscitation + 3 h: 11 ± 3 vs 8 ± 3 perfused vessels, p   〈  0.05). Conclusion Hemorrhagic shock-induced renal impairment cannot be restored by standard fluid resuscitation, nor by activation of Tie2. Future treatment strategies should focus on reducing angiopoietin-2 levels or on activating Tie2 via an alternative strategy.
    Type of Medium: Online Resource
    ISSN: 2197-425X
    URL: Article
    DOI: 10.1186/s40635-021-00389-5
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2740385-3
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