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CURRENT ISSUEMINERVA ANESTESIOLOGICA

A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care

Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 2,036

Frequency: Monthly

ISSN 0375-9393

Online ISSN 1827-1596

 

Minerva Anestesiologica 2016 May;82(5):525-33

    ORIGINAL ARTICLES

Blood-brain barrier permeability following traumatic brain injury

Mårten JUNGNER 1, Roger SIEMUND 2, Daniele VENTUROLI 1, Peter REINSTRUP 1, Wilhelm SCHALÉN 3, Peter BENTZER 1

1 Department of Anesthesiology and Intensive Care, Lund University and Skåne University Hospital, Lund, Sweden; 2 Department of Radiology, Lund University and Skåne University Hospital, Lund, Sweden; 3 Department of Neurosurgery, Lund University and Skåne University Hospital, Lund, Sweden

BACKGROUND: Brain edema and intracranial hypertension is deleterious after traumatic brain injury (TBI), but the underlying pathophysiology is complex and poorly understood. One major subject of controversy is the time course and extent of blood-brain barrier (BBB) dysfunction following trauma, and previous studies in humans have only provided semi-quantitative data. The objective of the present study was therefore to quantify changes in BBB-permeability in the early course of TBI, when brain edema is still evolving.
METHODS: Sixteen non-consecutive brain trauma patients and two controls were included. Following i.v. injection of iohexol and CT perfusion scans, patients were scanned eight times from 4 to 25 minutes. Blood to brain transfer constant (Ki) for iohexol (molecular weight 821 D), reflecting permeability and available area for diffusion, was calculated offline by Patlak plot analysis of the enhancement curves of intracerebral large venous vessels and pericontusional brain parenchyma.
RESULTS: In non-ischemic tissue surrounding contusions and hematomas Ki was increased 2- to 10-fold compared to normal tissue, reaching maximal values of 0.5 mL/min/100 g. In non-injured areas and in controls Ki was about 0.06 mL/min/100 g. The increase was more pronounced in the most severely injured patients, and was detectable within 24 hours after trauma and up to five days after.
CONCLUSIONS: Our results suggest that traumatic brain injury is associated with early focal increases in small molecular BBB-permeability. The results indicate that in the injured brain, capillary hydrostatic and oncotic pressures may influence edema formation.

language: English


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