دورية أكاديمية

Intravenous fluid resuscitation is associated with septic endothelial glycocalyx degradation.

التفاصيل البيبلوغرافية
العنوان: Intravenous fluid resuscitation is associated with septic endothelial glycocalyx degradation.
المؤلفون: Hippensteel JA; Department of Medicine, University of Colorado Denver, Aurora, CO, USA., Uchimido R; Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA., Tyler PD; Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA., Burke RC; Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA., Han X; Departments of Chemistry and Chemical Biology, Chemical and Biological Engineering, and Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, USA., Zhang F; Departments of Chemistry and Chemical Biology, Chemical and Biological Engineering, and Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, USA., McMurtry SA; Department of Medicine, University of Colorado Denver, Aurora, CO, USA., Colbert JF; Department of Medicine, University of Colorado Denver, Aurora, CO, USA., Lindsell CJ; Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA., Angus DC; Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA., Kellum JA; Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA., Yealy DM; Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, PA, USA., Linhardt RJ; Departments of Chemistry and Chemical Biology, Chemical and Biological Engineering, and Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, USA., Shapiro NI; Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA., Schmidt EP; Department of Medicine, University of Colorado Denver, Aurora, CO, USA. eric.schmidt@ucdenver.edu.; Department of Medicine, Denver Health Medical Center, Denver, CO, USA. eric.schmidt@ucdenver.edu.
المصدر: Critical care (London, England) [Crit Care] 2019 Jul 23; Vol. 23 (1), pp. 259. Date of Electronic Publication: 2019 Jul 23.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: BioMed Central Ltd Country of Publication: England NLM ID: 9801902 Publication Model: Electronic Cited Medium: Internet ISSN: 1466-609X (Electronic) Linking ISSN: 13648535 NLM ISO Abbreviation: Crit Care Subsets: MEDLINE
أسماء مطبوعة: Publication: London, UK : BioMed Central Ltd
Original Publication: London : Current Science Ltd, c1997-
مواضيع طبية MeSH: Endothelium/*physiopathology , Fluid Therapy/*adverse effects , Glycocalyx/*drug effects , Sepsis/*drug therapy, Administration, Intravenous ; Adult ; Aged ; Angiopoietin-2/analysis ; Angiopoietin-2/blood ; Atrial Natriuretic Factor/analysis ; Atrial Natriuretic Factor/blood ; Biomarkers/analysis ; Biomarkers/blood ; Endothelium/drug effects ; Endothelium/metabolism ; Female ; Fluid Therapy/methods ; Fluid Therapy/statistics & numerical data ; Glycocalyx/metabolism ; Heparitin Sulfate/analysis ; Heparitin Sulfate/blood ; Humans ; Male ; Mass Spectrometry/methods ; Middle Aged ; Natriuretic Peptide, Brain/analysis ; Natriuretic Peptide, Brain/blood ; Resuscitation/adverse effects ; Resuscitation/methods ; Resuscitation/statistics & numerical data ; Sepsis/blood ; Sepsis/physiopathology ; Syndecan-1/analysis ; Syndecan-1/blood ; Thrombomodulin/analysis ; Thrombomodulin/blood ; Tissue Plasminogen Activator/analysis ; Tissue Plasminogen Activator/blood ; Vascular Endothelial Growth Factor Receptor-1/analysis ; Vascular Endothelial Growth Factor Receptor-1/blood
مستخلص: Background: Intravenous fluids, an essential component of sepsis resuscitation, may paradoxically worsen outcomes by exacerbating endothelial injury. Preclinical models suggest that fluid resuscitation degrades the endothelial glycocalyx, a heparan sulfate-enriched structure necessary for vascular homeostasis. We hypothesized that endothelial glycocalyx degradation is associated with the volume of intravenous fluids administered during early sepsis resuscitation.
Methods: We used mass spectrometry to measure plasma heparan sulfate (a highly sensitive and specific index of systemic endothelial glycocalyx degradation) after 6 h of intravenous fluids in 56 septic shock patients, at presentation and after 24 h of intravenous fluids in 100 sepsis patients, and in two groups of non-infected patients. We compared plasma heparan sulfate concentrations between sepsis and non-sepsis patients, as well as between sepsis survivors and sepsis non-survivors. We used multivariable linear regression to model the association between volume of intravenous fluids and changes in plasma heparan sulfate.
Results: Consistent with previous studies, median plasma heparan sulfate was elevated in septic shock patients (118 [IQR, 113-341] ng/ml 6 h after presentation) compared to non-infected controls (61 [45-79] ng/ml), as well as in a second cohort of sepsis patients (283 [155-584] ng/ml) at emergency department presentation) compared to controls (177 [144-262] ng/ml). In the larger sepsis cohort, heparan sulfate predicted in-hospital mortality. In both cohorts, multivariable linear regression adjusting for age and severity of illness demonstrated a significant association between volume of intravenous fluids administered during resuscitation and plasma heparan sulfate. In the second cohort, independent of disease severity and age, each 1 l of intravenous fluids administered was associated with a 200 ng/ml increase in circulating heparan sulfate (p = 0.006) at 24 h after enrollment.
Conclusions: Glycocalyx degradation occurs in sepsis and septic shock and is associated with in-hospital mortality. The volume of intravenous fluids administered during sepsis resuscitation is independently associated with the degree of glycocalyx degradation. These findings suggest a potential mechanism by which intravenous fluid resuscitation strategies may induce iatrogenic endothelial injury.
References: Crit Care Med. 2000 Jan;28(1):74-8. (PMID: 10667502)
Intensive Care Med. 2003 Oct;29(10):1696-702. (PMID: 12915939)
Am J Physiol Heart Circ Physiol. 2005 Nov;289(5):H1993-9. (PMID: 15964925)
Crit Care Med. 1992 Jun;20(6):864-74. (PMID: 1597042)
Crit Care Med. 2006 Feb;34(2):344-53. (PMID: 16424713)
Arterioscler Thromb Vasc Biol. 2006 Aug;26(8):1784-90. (PMID: 16709945)
Anesthesiology. 2007 Nov;107(5):776-84. (PMID: 18073553)
Blood. 2010 Mar 25;115(12):2449-57. (PMID: 20097882)
Intensive Care Med. 2011 Jan;37(1):86-96. (PMID: 20924555)
Crit Care Med. 2011 Feb;39(2):259-65. (PMID: 20975548)
N Engl J Med. 2011 Jun 30;364(26):2483-95. (PMID: 21615299)
Ann Intensive Care. 2011 Nov 01;1(1):44. (PMID: 22044529)
Nat Med. 2012 Aug;18(8):1217-23. (PMID: 22820644)
Basic Res Cardiol. 2013 May;108(3):347. (PMID: 23563917)
J Intensive Care Med. 2014 Jul-Aug;29(4):213-7. (PMID: 23753235)
Acta Anaesthesiol Scand. 2014 Jan;58(1):36-43. (PMID: 24341693)
J Biol Chem. 2014 Mar 21;289(12):8194-202. (PMID: 24509853)
N Engl J Med. 2014 May 1;370(18):1683-93. (PMID: 24635773)
Crit Care. 2014 Oct 13;18(5):538. (PMID: 25497357)
Biochem Biophys Res Commun. 2015 May 8;460(3):596-602. (PMID: 25800869)
Anal Chem. 2015 Jun 16;87(12):6220-7. (PMID: 26005898)
Crit Care. 2015 Jun 15;19:251. (PMID: 26073560)
Am J Respir Crit Care Med. 2016 Aug 15;194(4):439-49. (PMID: 26926297)
Am J Physiol Heart Circ Physiol. 2016 Jun 1;310(11):H1468-78. (PMID: 27037369)
Sci Transl Med. 2016 Apr 20;8(335):335ra55. (PMID: 27099174)
Clin Chest Med. 2016 Jun;37(2):263-75. (PMID: 27229643)
Intensive Care Med. 2017 Feb;43(2):155-170. (PMID: 27734109)
Ann Intensive Care. 2017 Dec;7(1):4. (PMID: 28050897)
Chest. 2017 Jul;152(1):22-31. (PMID: 28109962)
Intensive Care Med. 2017 May;43(5):625-632. (PMID: 28130687)
Am J Respir Cell Mol Biol. 2017 Jun;56(6):727-737. (PMID: 28187268)
JAMA. 2017 Oct 3;318(13):1233-1240. (PMID: 28973227)
Ann Intensive Care. 2017 Oct 6;7(1):102. (PMID: 28986821)
Anaesth Intensive Care. 2017 Nov;45(6):737-743. (PMID: 29137585)
N Engl J Med. 2018 Mar 1;378(9):829-839. (PMID: 29485925)
Am J Respir Cell Mol Biol. 2018 Sep;59(3):363-374. (PMID: 29584451)
Ann Emerg Med. 2018 Oct;72(4):457-466. (PMID: 29753517)
Am J Respir Crit Care Med. 2018 Oct 15;198(8):1043-1054. (PMID: 29882682)
Am J Respir Crit Care Med. 2018 Oct 15;198(8):981-983. (PMID: 29940124)
Crit Care. 2018 Nov 20;22(1):308. (PMID: 30458880)
Crit Care. 2019 Jan 17;23(1):16. (PMID: 30654825)
PLoS One. 2019 Mar 27;14(3):e0213097. (PMID: 30917159)
Am J Pathol. 2019 Aug;189(8):1526-1535. (PMID: 31108101)
Intensive Care Med. 1996 Jul;22(7):707-10. (PMID: 8844239)
معلومات مُعتمدة: K08 AG061144 United States AG NIA NIH HHS; R01 HL125371 United States HL NHLBI NIH HHS; R03 AG056353 United States AG NIA NIH HHS
فهرسة مساهمة: Keywords: Endothelial glycocalyx; Fluid resuscitation; Multiple organ failure; Sepsis
المشرفين على المادة: 0 (ANGPT2 protein, human)
0 (Angiopoietin-2)
0 (Biomarkers)
0 (SDC1 protein, human)
0 (Syndecan-1)
0 (Thrombomodulin)
114471-18-0 (Natriuretic Peptide, Brain)
85637-73-6 (Atrial Natriuretic Factor)
9050-30-0 (Heparitin Sulfate)
EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
EC 3.4.21.68 (Tissue Plasminogen Activator)
تواريخ الأحداث: Date Created: 20190725 Date Completed: 20200129 Latest Revision: 20220408
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC6652002
DOI: 10.1186/s13054-019-2534-2
PMID: 31337421
قاعدة البيانات: MEDLINE
الوصف
تدمد:1466-609X
DOI:10.1186/s13054-019-2534-2