Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2000
The effects of dopamine on edema formation in two models of traumatic brain injury.
The risk of vasopressors worsening cerebral edema has been raised. Previously we have reported that dopamine was able to restore cerebral blood flow in a model of monotonically rising intracranial pressure. In this study the effects of dopamine on cortical contusion and diffuse injury with secondary insult are examined. ⋯ Dopamine however significantly worsened edema in ipsilateral and contralateral hippocampus and both temporal cortices. ADC remained unchanged except in the contralateral hippocampus where both water content and ADC rose with dopamine suggesting precipitation of a vasogenic edema. In this study dopamine clearly worsened edema formation in two models of traumatic brain injury, and we conclude that there may be analogous clinical situations; therefore pressors should not be considered a 'blanket' therapy for all patients with a low cerebral perfusion pressure.
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Acta Neurochir. Suppl. · Jan 2000
Assessment of 2-chloroadenosine treatment after experimental traumatic brain injury in the rat using arterial spin-labeled MRI: a preliminary report.
Adenosine is a putative endogenous neuroprotectant. Its action at A1 receptors mitigates excitotoxicity while action at A2 receptors increases cerebral blood flow (CBF). We hypothesized that cerebral injection of the adenosine analog, 2-chloroadenosine, would decrease swelling and increase CBF early after experimental traumatic brain injury (TBI). ⋯ In normal rats, injection of 0.3 nmole of 2-chloroadenosine did not increase CBF, but the higher dosage of 6 nmole dramatically increased hemispheric CBF by 1.5-2.0-fold. The effect of local injection of 2-chloroadenosine at a dose of 0.3 nmole after experimental TBI on Tlobs presumably represents a reduction in post-traumatic edema. This reduction in edema, along with the augmentation of CBF seen in normal rats at higher dosage (6 nmole), supports a role for adenosine in neuroprotection following TBI.
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Acta Neurochir. Suppl. · Jan 2000
Evidence for lactate uptake after rat fluid percussion brain injury.
Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Glucose declines and lactate increases after TBI as demonstrated in clinical and lab studies, suggesting increased glycolysis. This led us to hypothesize that high extracellular fluid (ECF) lactate may be beneficial after TBI. We measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before & after rat Fluid Percussion Injury (FPI) (2.06 +/- 0.13 atm) with and without i.v. lactate infusion (100 mM x 4.5 hours) to test the hypotheses that arterial lactate determines ECF lactate. 14C-lactate autoradiography was also performed, to demonstrate whether lactate is taken up by traumatized brain. ⋯ Dialysate lactate was always significantly higher than arterial. After lactate infusion, both the dialysate and the arterial lactate were significantly increased (P < 0.0001). Dialysate lactate increased within 10 min. following FPI, with significantly higher values in the lactate infusion group (82% higher with lactate infusion after FPI). Dialysate glucose fell following FPI, with a more severe decline in the saline group (129% lower), suggesting lactate infusion preserves or "spares" glucose in ECF. In our autoradiographic study, i.v. 14C-lactate accumulated at the injury site, with levels 2-4 times higher than in contralateral cortex. In conclusion, arterial lactate augmentation thus increases brain dialysate lactate and results in less reduction in ECF glucose, after FPI. Infused lactate accumulates at the injury site, where metabolism is probably the greatest.
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Acta Neurochir. Suppl. · Jan 1999
ReviewThe role of transcranial Doppler in the management of patients with subarachnoid haemorrhage--a review.
Introduced 15 years ago, transcranial Doppler (TCD) recordings of blood-velocity in patients with recent subarachnoid haemorrhage (SAH) have two objectives: to detect elevated blood velocities suggesting cerebral vasospasm (VSP) and to identify patients at risk for delayed cerebral ischemic deficits (DID). The pathophysiological cascade causing DID is complex. Discrepancies between blood velocities and DID (presuming that there actually is an "ischemic threshold" for blood velocity in absolute terms, which seems most unlikely) have been demonstrated, particularly in patients with elevated intracranial pressure (ICP) levels. ⋯ This probably explains why the clinical value of TCD is still debated. There is still uncertainty as to the best method to prevent and to treat VSP, and the overall outcome after SAH depends on so many factors besides VSP. Conclusive evidence may therefore be hard to obtain, and it appears sound to conclude that even with advanced investigation technology available, proper selection, pre- peri- and postoperative care and timing of surgery remain cornerstones in the management of these patients,--equal in importance to their treatment in the operating room or in the interventional angiography suite.
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This paper briefly reviews some basic principles of neurosurgical intensive care of patients with aneurysmal subarachnoid hemorrhage. The importance of early identification of secondary insults are underlined. Special attention is paid to the newly introduced method for neurochemical monitoring by means of intracerebral microdialysis. It is concluded that a well functioning neurointensive care unit constitutes an important organisational frame for the detection, prevention and treatment of secondary insults, after aneurysmal subarachnoidal hemorrhage and that improved results can be expected by applying a modern neurointensive care strategy also for patients with aneurysmal subarachnoid hemorrhage.