Abstract
BackgroundCerebral injury may alter the autoregulation of cerebral blood flow. One index for describing cerebrovascular state is the pressure reactivity (PR). Little is known of whether PR is associated with measures of brain metabolism and indicators of ischemia and cell damage. The aim of this investigation was to explore whether increased interstitial levels of glycerol, a marker of cell membrane damage, are associated with PR, and if prostacyclin, a membrane stabilizer and regulator of the microcirculation, may affect this association in a beneficial way.Materials and MethodsPatients suffering severe traumatic brain injury (sTBI) were treated according to an intracranial pressure (ICP)-targeted therapy based on the Lund concept and randomized to an add-on treatment with prostacyclin or placebo. Inclusion criteria were verified blunt head trauma, Glasgow Coma Score ≤ 8, age 15–70 years, and a first measured cerebral perfusion pressure of ≥ 10 mmHg. Multimodal monitoring was applied. A brain microdialysis catheter was placed on the worst affected side, close to the penumbra zone. Mean (glycerolmean) and maximal glycerol (glycerolmax) during the 96-h sampling period were calculated. The mean PR was calculated as the ICP/mean arterial pressure (MAP) regression coefficient based on hourly mean ICP and MAP during the first 96 h.ResultsOf the 48 included patients, 45 had valid glycerol and PR measurements available. PR was higher in the placebo group as compared to the prostacyclin group (p = 0.0164). There was a positive correlation between PR and the glycerolmean (ρ = 0.503, p = 0.01) and glycerolmax (ρ = 0.490, p = 0.015) levels in the placebo group only.ConclusionsPR is correlated to the glycerol level in patients suffering from sTBI, a relationship that is not seen in the group treated with prostacyclin. Glycerol has been associated with membrane degradation and may support glycerol as a biomarker for vascular endothelial breakdown. Such a breakdown may impair the regulation of cerebrovascular PR.
Highlights
Cerebral injury may affect the autoregulation of cerebral blood flow (CBFAR)
pressure reactivity (PR) is correlated to the glycerol level in patients suffering from severe traumatic brain injury (sTBI), a relationship that is not seen in the group treated with prostacyclin
There was no significant difference between the placebo and prostacyclin groups concerning mean arterial blood pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), Glasgow Coma Score (GCS), injury severity score (ISS), time to first computed tomography (CT), Rotterdam score, proportion or timing of hemicraniectomy, Glasgow Outcome Scale Extended, and mortality at 6 months or lactate/pyruvate ratio during the 96 h, see Table 1
Summary
Cerebral injury may affect the autoregulation of cerebral blood flow (CBFAR). it is important in traumaticA central function of cerebral pressure autoregulation is the ability to maintain a stable intracranial pressure (ICP) for a wide range of mean arterial blood pressure (MAP) levels. Cerebral injury may affect the autoregulation of cerebral blood flow (CBFAR). A central function of cerebral pressure autoregulation is the ability to maintain a stable intracranial pressure (ICP) for a wide range of mean arterial blood pressure (MAP) levels. We implemented the PR-method by Howell et al [1] They assessed the patient’s ability to maintain a stable ICP for a wide range of MAP levels by calculating the correlation between hourly mean ICP and MAP values. If ICP was stable over a wide range of MAP levels, the patient was described as pressure stable. The aim of this investigation was to explore whether increased interstitial levels of glycerol, a marker of cell membrane damage, are associated with PR, and if prostacyclin, a membrane stabilizer and regulator of the microcirculation, may affect this association in a beneficial way
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