Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma

Charles E Wade, Nena Matijevic, Yao Wei W. Wang, Erika G. Rodriguez, Ernesto Lopez, Sisse R. Ostrowski, Jessica C Cardenas, Lisa A. Baer, Tzu An Chen, Jeffrey S. Tomasek, Hanne H. Henriksen, Jakob Stensballe, Bryan A Cotton, John B Holcomb, Pär I. Johansson

Research output: Contribution to journalArticle

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Abstract

INTRODUCTION: Severe trauma is accompanied by endothelial glycocalyx disruption, which drives coagulopathy, increasing transfusion requirements and death. This syndrome has been termed endotheliopathy of trauma (EOT). Some have suggested EOT results from endothelial cellular damage and apoptosis. Endothelial microvesicles (EMVs) represent cellular damage. We hypothesized that EOT is associated with endothelial damage and apoptosis resulting in an increase in circulating EMVs. METHODS: Prospective, observational study enrolling severely injured patients. Twelve patients with EOT, based on elevated Syndecan-1 levels, were matched with 12 patients with lower levels, based on Injury Severity Score (ISS), abbreviated injury scale profile, and age. Thrombelastography and plasma levels of biomarkers indicative of cellular damage were measured from blood samples collected on admission. EMVs were determined by flow cytometry using varied monoclonal antibodies associated with endothelial cells. Significance was set at P < 0.05. RESULTS: Admission physiology and ISS (29 vs. 28) were similar between groups. Patients with EOT had higher Syndecan-1, 230 (158, 293) vs. 19 (14, 25) ng/mL, epinephrine, and soluble thrombomodulin levels. Based on thrombelastography, EOT had reductions in clot initiation, amplification, propagation and strength, and a greater frequency of transfusion, 92% vs. 33%. There were no differences in EMVs irrespective of the antibody used. Plasma norepinephrine, sE-selectin, sVE-cadherin, and histone-complexed DNA fragments levels were similar. CONCLUSION: In trauma patients presenting with EOT, endothelial cellular damage or apoptosis does not seem to occur based on the absence of an increase in EMVs and other biomarkers. Thus, this suggests endothelial glycocalyx disruption is the underlying primary cause of EOT.

LanguageEnglish
Pages180-184
Number of pages5
JournalShock (Augusta, Ga.)
Volume51
Issue number2
DOIs
StatePublished - Feb 1 2019

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Wounds and Injuries
Syndecan-1
Thrombelastography
Glycocalyx
Injury Severity Score
Apoptosis
Biomarkers
Abbreviated Injury Scale
Thrombomodulin
Selectins
Cadherins
Histones
Epinephrine
Observational Studies
Norepinephrine
Flow Cytometry
Endothelial Cells
Monoclonal Antibodies
Prospective Studies
Antibodies

ASJC Scopus subject areas

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Wade, C. E., Matijevic, N., Wang, Y. W. W., Rodriguez, E. G., Lopez, E., Ostrowski, S. R., ... Johansson, P. I. (2019). Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma. Shock (Augusta, Ga.), 51(2), 180-184. https://doi.org/10.1097/SHK.0000000000001149

Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma. / Wade, Charles E; Matijevic, Nena; Wang, Yao Wei W.; Rodriguez, Erika G.; Lopez, Ernesto; Ostrowski, Sisse R.; Cardenas, Jessica C; Baer, Lisa A.; Chen, Tzu An; Tomasek, Jeffrey S.; Henriksen, Hanne H.; Stensballe, Jakob; Cotton, Bryan A; Holcomb, John B; Johansson, Pär I.

In: Shock (Augusta, Ga.), Vol. 51, No. 2, 01.02.2019, p. 180-184.

Research output: Contribution to journalArticle

Wade, CE, Matijevic, N, Wang, YWW, Rodriguez, EG, Lopez, E, Ostrowski, SR, Cardenas, JC, Baer, LA, Chen, TA, Tomasek, JS, Henriksen, HH, Stensballe, J, Cotton, BA, Holcomb, JB & Johansson, PI 2019, 'Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma', Shock (Augusta, Ga.), vol. 51, no. 2, pp. 180-184. https://doi.org/10.1097/SHK.0000000000001149
Wade CE, Matijevic N, Wang YWW, Rodriguez EG, Lopez E, Ostrowski SR et al. Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma. Shock (Augusta, Ga.). 2019 Feb 1;51(2):180-184. https://doi.org/10.1097/SHK.0000000000001149
Wade, Charles E ; Matijevic, Nena ; Wang, Yao Wei W. ; Rodriguez, Erika G. ; Lopez, Ernesto ; Ostrowski, Sisse R. ; Cardenas, Jessica C ; Baer, Lisa A. ; Chen, Tzu An ; Tomasek, Jeffrey S. ; Henriksen, Hanne H. ; Stensballe, Jakob ; Cotton, Bryan A ; Holcomb, John B ; Johansson, Pär I. / Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma. In: Shock (Augusta, Ga.). 2019 ; Vol. 51, No. 2. pp. 180-184.
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N2 - INTRODUCTION: Severe trauma is accompanied by endothelial glycocalyx disruption, which drives coagulopathy, increasing transfusion requirements and death. This syndrome has been termed endotheliopathy of trauma (EOT). Some have suggested EOT results from endothelial cellular damage and apoptosis. Endothelial microvesicles (EMVs) represent cellular damage. We hypothesized that EOT is associated with endothelial damage and apoptosis resulting in an increase in circulating EMVs. METHODS: Prospective, observational study enrolling severely injured patients. Twelve patients with EOT, based on elevated Syndecan-1 levels, were matched with 12 patients with lower levels, based on Injury Severity Score (ISS), abbreviated injury scale profile, and age. Thrombelastography and plasma levels of biomarkers indicative of cellular damage were measured from blood samples collected on admission. EMVs were determined by flow cytometry using varied monoclonal antibodies associated with endothelial cells. Significance was set at P < 0.05. RESULTS: Admission physiology and ISS (29 vs. 28) were similar between groups. Patients with EOT had higher Syndecan-1, 230 (158, 293) vs. 19 (14, 25) ng/mL, epinephrine, and soluble thrombomodulin levels. Based on thrombelastography, EOT had reductions in clot initiation, amplification, propagation and strength, and a greater frequency of transfusion, 92% vs. 33%. There were no differences in EMVs irrespective of the antibody used. Plasma norepinephrine, sE-selectin, sVE-cadherin, and histone-complexed DNA fragments levels were similar. CONCLUSION: In trauma patients presenting with EOT, endothelial cellular damage or apoptosis does not seem to occur based on the absence of an increase in EMVs and other biomarkers. Thus, this suggests endothelial glycocalyx disruption is the underlying primary cause of EOT.

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