34 research outputs found
Pichler, F.: Die Urbare, urbariale Aufzeichnungen und Grundbücher der Steiermark. Bd. 3/II K-R
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The Role of Excitatory Amino Acids in Severe Brain Trauma: Opportunities for Therapy: A Review
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Brain Oxygen, CO2, pH, and Temperature Monitoring Evaluation in the Feline Brain
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Brain oxygenation and energy metabolism: part I-biological function and pathophysiology
CONTINUOUS OXYGEN DELIVERY and CO(2) clearance are paramount in the maintenance of normal brain function and tissue integrity. Under normal conditions, aerobic metabolism is the major source of energy in the brain, but this system may be compromised by the interruption of substrate delivery and disturbances in cerebral metabolism. These disruptions are major factors contributing to ischemic and hypoxic brain damage resulting from traumatic brain injury, stroke, and subarachnoid hemorrhage. There is evidence that mitochondrial function also is reduced after injury. Furthermore, early impairment of cerebral blood flow in patients with severe injury correlates with poor tissue oxygenation and may be an important parameter in secondary damage. Recent advances in brain tissue monitoring in the intensive care unit and operating room have made it possible to continuously measure tissue oxygen tension and temperature, as well as certain aspects of brain metabolism and neurochemistry. Therefore, it is important to understand the physiological process and the pathophysiology produced by these events. This is Part I of a two-part review that analyzes the physiology of cerebral oxygenation and metabolism as well as some of the pathological mechanisms involved in ischemic and traumatic brain injuries. Brain tissue monitoring techniques will be examined in the second article of this two-part series. To understand cerebral oxygenation, it is important to understand cerebral blood flow, energy production, ischemia, acidosis, generation of reactive oxygen species, and mitochondrial failure. These issues provide the basis of knowledge regarding brain bioenergetics and are important topics to understand when developing new approaches to patient care
Glutamate Release and Cerebral Blood Flow After Severe Human Head Injury
Elevations of extracellular glutamate have been found in patients with prolonged brain ischemia and focal cerebral contusions, following severe head injury. About 30% of severely head injured patients develop cerebral ischemia, defined as CBF < 18 ml/100g/min. Patients with both global and regional cerebral ischemia have the worst outcome. However, the relationship between CBF and EAA release is not well understood in head injured humans, and may differ from the findings in normal animals. To study the relationship between EAA release and CBF after severe head injury, we performed cerebral blood flow measurements using stable xenon enhanced computed tomography and correlated these with glutamate release in the extracellular fluid, measured by continuous microdialysis, in 25 severely head injured patients.
Sustained cerebral blood flow reductions below the threshold for ischemic neuronal damage was closely related to massive excitatory amino acid release, as in previous animal studies. In patients without secondary ischemia, or focal contusions, delayed post-traumatic glutamate release appeared to be only transient or did not occur at all
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Does continuous measurement of brain tissue temperature reflect cerebral blood flow in the severely head injured patients?
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Does brain nitric oxide generation influence tissue oxygenation after severe human subarachnoid hemorrhage?
IntroductionNitric oxide (NO) is now believed to be involved in many physiological events, especially vasoregulation. In the brain, NO has been implicated in retrograde neurotransmission, synaptic plasticity and vasomotor control. NO leads to vasodilation by diffusing across all membranes, and interrelates with guanylate cyclase in the smooth muscle, as its primary receptor target, thus regulating cerebral perfusion and cerebral blood flow (CBF). NO is rapidly synthesized on demand by nitric oxide synthase (NOS), which is present in a wide variety of tissues, including endothelial cells. Three isoforms of NOS are described, and all of them are expressed in the brain. The constitutive, endothelial and neuronal NOSs are believed to be primarily responsible for cerebral perfusion.In neurons, NO release is stimulated by the excitatory amino acid glutamate via N-methyl-d-aspartate receptors. The NO then acts as a retrograde or orthodox neurotransmitter. Endothelial cells may supply tonically released NO that influences cerebral resistance vessels; however, the presence of NOS in glial and neuronal cells makes it likely that the coupling of CBF and neuronal activity is achieved via NO activity. The vasodilatory function of NO may be reduced after subarachnoid hemorrhage (SAH), due to reduced NO production or a disturbance of the basal vasomotor balance. Endothelial NO is profoundly reduced in some forms of experimental ischemia, leading to compensatory induction of NOS. Hemoglobin derived from the blood and oxyhemoglobin in the subarachnoid space (after SAH) binds to NO, thereby reducing its vasodilating effect
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Association between elevated brain tissue glycerol levels and poor outcome following severe traumatic brain injury
OBJECT: Glycerol is considered to be a marker of cell membrane degradation and thus cellular lysis. Recently, it has become feasible to measure via microdialysis cerebral extracellular fluid (ECF) glycerol concentrations at the patient's bedside. Therefore the aim of this study was to investigate the ECF concentration and time course of glycerol after severe traumatic brain injury (TBI) and its relationship to patient outcome and other monitoring parameters. METHODS: As soon as possible after injury for up to 4 days, 76 severely head-injured patients were monitored using a microdialysis probe (cerebral glycerol) and a Neurotrend sensor (brain tissue PO2) in uninjured brain tissue confirmed by computerized tomography scanning. The mean brain tissue glycerol concentration in all monitored patients decreased significantly from 206 +/- 31 micromol/L on Day 1 to 9 +/- 3 micromol/L on Day 4 after injury (p < 0.0001). Note, however, that there was no significant difference in the time course between patients with a favorable outcome (Glasgow Outcome Scale [GOS] Scores 4 and 5) and those with an unfavorable outcome (GOS Scores 1-3). Significantly increased glycerol concentrations were observed when brain tissue PO2 was less than 10 mm Hg or when cerebral perfusion pressure was less than 70 mm Hg. CONCLUSIONS: Based on results in the present study one can infer that microdialysate glycerol is a marker of severe tissue damage, as seen immediately after brain injury or during profound tissue hypoxia. Given that brain tissue glycerol levels do not yet add new clinically significant information, however, routine monitoring of this parameter following traumatic brain injury needs further validation
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