Is all plasma created equal? A pilot study of the effect of interdonor variability.
Adolescent
Adult
Aged
Aged, 80 and over
Animals
Biological Variation, Population
/ physiology
Blood Component Transfusion
/ adverse effects
Blood Donors
Cell Membrane Permeability
Cytokines
/ metabolism
Disease Models, Animal
Electric Impedance
Endothelial Cells
/ cytology
Female
Healthy Volunteers
Humans
Lung
/ cytology
Lung Injury
/ etiology
Male
Middle Aged
Pilot Projects
Plasma
/ metabolism
Resuscitation
/ adverse effects
Shock, Hemorrhagic
/ complications
Young Adult
Journal
The journal of trauma and acute care surgery
ISSN: 2163-0763
Titre abrégé: J Trauma Acute Care Surg
Pays: United States
ID NLM: 101570622
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
pubmed:
7
11
2019
medline:
25
6
2020
entrez:
6
11
2019
Statut:
ppublish
Résumé
Clinical benefits of plasma as an adjunct for treatment of hemorrhagic shock (HS) have been well established. However, its use is not without risk. Little is understood regarding the clinical implications of plasma variability. We hypothesized there to be interdonor variability in plasma that would impact endothelial and organ function postinjury. Pulmonary endothelial cells (ECs) were incubated with plasma from 24 random donors, and transendothelial electrical resistance was measured. Plasma units with a more or less protective effect on reducing EC permeability were selected for testing in vivo. Syndecan-1 and cytokines were measured. Mice underwent laparotomy and then HS followed by resuscitation with the selected plasma units and were compared with mice receiving no resuscitation and shams. Lung tissue was sectioned and stained for myeloperoxidase and pulmonary syndecan-1 and scored for lung histopathologic injury. Plasma from 24 donors revealed variability in the reversal of EC monolayer hyperpermeability; transendothelial electrical resistance for the more protective plasma was significantly higher than that for the less protective plasma (0.801 ± 0.022 vs. 0.744 ± 0.035; p = 0.002). Syndecan-1 was also markedly increased in the less protective compared with the more protective plasma (38427 ± 1257 vs. 231 ± 172 pg/mL, p < 0.001), while cytokines varied. In vivo, the more protective plasma mitigated lung histopathologic injury compared with the less protective plasma (1.56 ± 0.27 vs. 2.33 ± 0.47, respectively; p = 0.005). Similarly, myeloperoxidase was significantly reduced in the more protective compared with the less protective plasma group (2.590 ± 0.559 vs. 6.045 ± 1.885; p = 0.02). Lastly, pulmonary syndecan-1 immunostaining was significantly increased in the more protective compared with the less protective plasma group (20.909 ± 8.202 vs. 9.325 ± 3.412; p = 0.018). These data demonstrate significant interdonor variability in plasma that can adversely influence the protective effects of plasma-based resuscitation on HS-induced lung injury. This may have important implications for patient safety and clinical outcomes.
Sections du résumé
BACKGROUND
Clinical benefits of plasma as an adjunct for treatment of hemorrhagic shock (HS) have been well established. However, its use is not without risk. Little is understood regarding the clinical implications of plasma variability. We hypothesized there to be interdonor variability in plasma that would impact endothelial and organ function postinjury.
METHODS
Pulmonary endothelial cells (ECs) were incubated with plasma from 24 random donors, and transendothelial electrical resistance was measured. Plasma units with a more or less protective effect on reducing EC permeability were selected for testing in vivo. Syndecan-1 and cytokines were measured. Mice underwent laparotomy and then HS followed by resuscitation with the selected plasma units and were compared with mice receiving no resuscitation and shams. Lung tissue was sectioned and stained for myeloperoxidase and pulmonary syndecan-1 and scored for lung histopathologic injury.
RESULTS
Plasma from 24 donors revealed variability in the reversal of EC monolayer hyperpermeability; transendothelial electrical resistance for the more protective plasma was significantly higher than that for the less protective plasma (0.801 ± 0.022 vs. 0.744 ± 0.035; p = 0.002). Syndecan-1 was also markedly increased in the less protective compared with the more protective plasma (38427 ± 1257 vs. 231 ± 172 pg/mL, p < 0.001), while cytokines varied. In vivo, the more protective plasma mitigated lung histopathologic injury compared with the less protective plasma (1.56 ± 0.27 vs. 2.33 ± 0.47, respectively; p = 0.005). Similarly, myeloperoxidase was significantly reduced in the more protective compared with the less protective plasma group (2.590 ± 0.559 vs. 6.045 ± 1.885; p = 0.02). Lastly, pulmonary syndecan-1 immunostaining was significantly increased in the more protective compared with the less protective plasma group (20.909 ± 8.202 vs. 9.325 ± 3.412; p = 0.018).
CONCLUSION
These data demonstrate significant interdonor variability in plasma that can adversely influence the protective effects of plasma-based resuscitation on HS-induced lung injury. This may have important implications for patient safety and clinical outcomes.
Identifiants
pubmed: 31688783
doi: 10.1097/TA.0000000000002529
pmc: PMC7055504
mid: NIHMS1549025
pii: 01586154-202001000-00016
doi:
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
121-127Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM107482
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM129533
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007698
Pays : United States
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