{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:49:11Z","timestamp":1773301751000,"version":"3.50.1"},"reference-count":45,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2000,11]]},"abstract":"<jats:p content-type=\"fine-print\"><jats:italic>Object.<\/jats:italic> Disturbed ionic and neurotransmitter homeostasis are now recognized as probably the most important mechanisms contributing to the development of secondary brain swelling after traumatic brain injury (TBI). Evidence obtained in animal models indicates that posttraumatic neuronal excitation by excitatory amino acids leads to an increase in extracellular potassium, probably due to ion channel activation. The purpose of this study was therefore to measure dialysate potassium in severely head injured patients and to correlate these results with measurements of intracranial pressure (ICP), patient outcome, and levels of dialysate glutamate and lactate, and cerebral blood flow (CBF) to determine the role of ischemia in this posttraumatic ion dysfunction.<\/jats:p><jats:p content-type=\"fine-print\"><jats:italic>Methods.<\/jats:italic> Eighty-five patients with severe TBI (Glasgow Coma Scale Score &lt; 8) were treated according to an intensive ICP management-focused protocol. All patients underwent intracerebral microdialyis. Dialysate potassium levels were analyzed using flame photometry, and dialysate glutamate and dialysate lactate levels were measured using high-performance liquid chromatography and an enzyme-linked amperometric method in 72 and 84 patients, respectively. Cerebral blood flow studies (stable xenon computerized tomography scanning) were performed in 59 patients.<\/jats:p><jats:p content-type=\"fine-print\">In approximately 20% of the patients, dialysate potassium values were increased (dialysate potassium &gt; 1.8 mM) for 3 hours or more. A mean amount of dialysate potassium greater than 2 mM throughout the entire monitoring period was associated with ICP above 30 mm Hg and fatal outcome, as were progressively rising levels of dialysate potassium. The presence of dialysate potassium correlated positively with dialysate glutamate (p &lt; 0.0001) and lactate (p &lt; 0.0001) levels. Dialysate potassium was significantly inversely correlated with reduced CBF (p = 0.019).<\/jats:p><jats:p content-type=\"fine-print\"><jats:italic>Conclusions.<\/jats:italic> Dialysate potassium was increased after TBI in 20% of measurements. High levels of dialysate potassium were associated with increased ICP and poor outcome. The simultaneous increase in dialysate potassium, together with dialysate glutamate and lactate, supports the concept that glutamate induces ionic flux and consequently increases ICP, which the authors speculate may be due to astrocytic swelling. Reduced CBF was also significantly correlated with increased levels of dialysate potassium. This may be due to either cell swelling or altered vasoreactivity in cerebral blood vessels caused by higher levels of potassium after trauma. Additional studies in which potassium-sensitive microelectrodes are used are needed to validate these ionic events more clearly.<\/jats:p>","DOI":"10.3171\/jns.2000.93.5.0800","type":"journal-article","created":{"date-parts":[[2009,5,13]],"date-time":"2009-05-13T17:27:13Z","timestamp":1242235633000},"page":"800-807","source":"Crossref","is-referenced-by-count":73,"title":["High level of extracellular potassium and its correlates after severe human head injury: relationship to high intracranial pressure"],"prefix":"10.3171","volume":"93","author":[{"given":"Michael","family":"Reinert","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ahmad","family":"Khaldi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alois","family":"Zauner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Egon","family":"Doppenberg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sung","family":"Choi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ross","family":"Bullock","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1754","reference":[{"key":"b1","series-title":"Brain Res","doi-asserted-by":"publisher","first-page":"190","DOI":"10.1016\/0006-8993(92)91206-T","article-title":"Functional compartmentalization of energy production in neural tissue.","volume":"585","author":"Andersen","year":"1992"},{"key":"b2","series-title":"Am J Physiol","first-page":"H1674","article-title":"ATP-dependent K+ channel activation reduces loss of opioid dilation after brain injury.","volume":"274","author":"Armstead","year":"1998"},{"key":"b3","series-title":"Brain Res","doi-asserted-by":"publisher","first-page":"177","DOI":"10.1016\/S0006-8993(97)00641-0","article-title":"Role of impaired cAMP and calcium-sensitive K+ channel function in altered cerebral hemodynamics following brain injury.","volume":"768","author":"Armstead","year":"1997"},{"key":"b4","series-title":"J Physiol","doi-asserted-by":"publisher","first-page":"159","DOI":"10.1113\/jphysiol.1987.sp016361","article-title":"Ion activities and potassium uptake mechanisms of glial cells in guinea pig olfactory cortex slices.","volume":"382","author":"Ballanyi","year":"1987"},{"key":"b5","series-title":"Glia","doi-asserted-by":"publisher","first-page":"151","DOI":"10.1002\/glia.440030302","article-title":"Electrophysiological measurements of volume changes in leech neuropile glial cells.","volume":"3","author":"Ballanyi","year":"1990"},{"key":"b6","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"507","DOI":"10.3171\/jns.1998.89.4.0507","article-title":"Factors affecting excitatory amino acid release following severe human head injury.","volume":"89","author":"Bullock","year":"1998"},{"key":"b7","series-title":"Neurochemical Monitoring in the Intensive Care Unit: Microdialysis, Jugular Venous Oximetry, and Near-Infrared Spectroscopy.","article-title":"Patterns of excitatory amino acid release and ionic flux after severe human head injury","author":"Bullock","year":"1995"},{"key":"b8","series-title":"J Neurotrauma","doi-asserted-by":"publisher","first-page":"497","DOI":"10.1089\/neu.1996.13.497","article-title":"Voltage-dependent Na+\/K+ ion channel blockade fails to ameliorate behavioral deficits after traumatic brain injury in the rat.","volume":"13","author":"Di","year":"1996"},{"key":"b9","series-title":"Dev Neurosci","doi-asserted-by":"publisher","first-page":"360","DOI":"10.1159\/000111429","article-title":"A role for astrocytes in glucose delivery to neurons?","volume":"18","author":"Forsyth","year":"1996"},{"key":"b10","series-title":"J Cereb Blood Flow Metab","doi-asserted-by":"publisher","first-page":"371","DOI":"10.1038\/jcbfm.1992.54","article-title":"The effect of MK-801 on cortical spreading depression in the penumbral zone following focal ischaemia in the rat.","volume":"12","author":"Gill","year":"1992"},{"key":"b11","series-title":"J Neurosci","doi-asserted-by":"publisher","first-page":"7367","DOI":"10.1523\/JNEUROSCI.19-17-07367.1999","article-title":"Enhancement of AMPA-mediated current after traumatic injury in cortical neurons.","volume":"19","author":"Goforth","year":"1999"},{"key":"b12","series-title":"Physiol Rev","doi-asserted-by":"publisher","first-page":"101","DOI":"10.1152\/physrev.1985.65.1.101","article-title":"Effect of anoxia on ion distribution in the brain.","volume":"65","author":"Hansen","year":"1985"},{"key":"b13","series-title":"Neurol Res","doi-asserted-by":"publisher","first-page":"94","DOI":"10.1080\/01616412.1995.11740294","article-title":"Inhibition of the high affinity glutamate uptake system facilitates the massive potassium flux during cerebral ischaemia in vivo.","volume":"17","author":"Hirota","year":"1995"},{"key":"b14","series-title":"Acta Physiol Scand","first-page":"437","article-title":"Cation activities in reversible ischemia in the rat brain cortex.","volume":"113","author":"Hossman","year":"1977"},{"key":"b15","series-title":"Lancet","first-page":"480","article-title":"Assessment of outcome after severe brain damage. A practical scale.","volume":"1","author":"Jennett","year":"1975"},{"key":"b16","series-title":"Am J Physiol","first-page":"2639","article-title":"Endothelin impairs ATP-sensitive K+ channel function after brain injury.","volume":"273","author":"Kasemsri","year":"1997"},{"key":"b17","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"889","DOI":"10.3171\/jns.1990.73.6.0889","article-title":"Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.","volume":"73","author":"Katayama","year":"1990"},{"key":"b18","series-title":"Brain Pathol","doi-asserted-by":"publisher","first-page":"427","DOI":"10.1111\/j.1750-3639.1995.tb00621.x","article-title":"Role of excitatory amino acid-mediated ionic fluxes in traumatic brain injury.","volume":"5","author":"Katayama","year":"1995"},{"key":"b19","series-title":"Acta Neurochir Suppl","first-page":"7","article-title":"Neuron-glial interaction during injury and edema of the CNS.","volume":"60","author":"Kempski","year":"1994"},{"key":"b20","series-title":"Ann NY Acad Sci","doi-asserted-by":"publisher","first-page":"306","DOI":"10.1111\/j.1749-6632.1991.tb15622.x","article-title":"Glial ion transport and volume control.","volume":"633","author":"Kempski","year":"1991"},{"key":"b21","series-title":"Proc R Soc Lond (B)","first-page":"1","article-title":"Neuroglial cells: physiological properties and a potassium mediated effect of neuronal activity on the glial membrane potential.","volume":"168","author":"Kuffler","year":"1967"},{"key":"b22","series-title":"J Neurochem","first-page":"1734","article-title":"Lactate metabolism and its effect on glucose metabolism in an excised neural tissue.","volume":"64","author":"Larrabee","year":"1995"},{"key":"b23","series-title":"J Neurochem","first-page":"1726","article-title":"Partitioning of CO2 production between glucose and lactate in excised sympathetic ganglia, with implications for brain.","volume":"67","author":"Larrabee","year":"1996"},{"key":"b24","series-title":"J Neurotrauma","first-page":"S463","article-title":"Cholinergic and opioid mediation of traumatic brain injury.","volume":"9","author":"Lyeth","year":"1992"},{"key":"b25","series-title":"Dev Neurosci","doi-asserted-by":"publisher","first-page":"306","DOI":"10.1159\/000111349","article-title":"Neurotransmitters regulate energy metabolism in astrocytes: implications for the metabolic trafficking between neural cells.","volume":"15","author":"Magistretti","year":"1993"},{"key":"b26","series-title":"Brain Res","doi-asserted-by":"publisher","first-page":"268","DOI":"10.1016\/S0006-8993(96)00874-8","article-title":"Cortical spreading depression recorded from human brain using a multiparametric monitioring system.","volume":"740","author":"Mayevsky","year":"1996"},{"key":"b27","series-title":"From Neuron to Brain: A Cellular and Molecular Approach to the Function of the Nervous System","author":"Nicholls","year":"1992"},{"key":"b28","series-title":"J Cereb Blood Flow Metab","doi-asserted-by":"publisher","first-page":"183","DOI":"10.1038\/jcbfm.1993.22","article-title":"Regional changes in interstitial K+ and Ca2+ levels following cortical compression contusion trauma in rats.","volume":"13","author":"Nilsson","year":"1993"},{"key":"b29","series-title":"Science","doi-asserted-by":"publisher","first-page":"896","DOI":"10.1126\/science.3616619","article-title":"Does the release of potassium from astrocytes endfeet regulate cerebral blood flow.","volume":"237","author":"Paulson","year":"1987"},{"key":"b30","series-title":"Proc Natl Acad Sci USA","doi-asserted-by":"publisher","first-page":"10625","DOI":"10.1073\/pnas.91.22.10625","article-title":"Glutamate uptake into astrocytes stimulates aerobic glycolisis: a mechanism coupling neuronal activity to glucose utilization.","volume":"91","author":"Pellerin","year":"1994"},{"key":"b31","series-title":"Dev Neurosci","doi-asserted-by":"publisher","first-page":"291","DOI":"10.1159\/000017324","article-title":"Evidence supporting the existence of an activity-dependent astrocyte-neuron lactate shuttle.","volume":"20","author":"Pellerin","year":"1998"},{"key":"b32","series-title":"Glia","doi-asserted-by":"publisher","first-page":"99","DOI":"10.1002\/(SICI)1098-1136(199709)21:1<99::AID-GLIA11>3.0.CO;2-W","article-title":"Trafficking between glia and neurons of TCA cycle intermediates and related metabolites.","volume":"21","author":"Schousboe","year":"1997"},{"key":"b33","series-title":"Neurosurgery","doi-asserted-by":"publisher","first-page":"1276","DOI":"10.1097\/00006123-199806000-00042","article-title":"Regional cerebral blood volume after severe head injury patients with regional cerebral ischemia.","volume":"42","author":"Schroder","year":"1998"},{"key":"b34","series-title":"J Neurosci","doi-asserted-by":"publisher","first-page":"34","DOI":"10.1523\/JNEUROSCI.19-01-00034.1999","article-title":"An increase in lactate output by brain tissue serves to meet the energy needs of glutamate-activated neurons.","volume":"19","author":"Schurr","year":"1999"},{"key":"b35","series-title":"Science","doi-asserted-by":"publisher","first-page":"1326","DOI":"10.1126\/science.3375817","article-title":"Lactate-supported synaptic function in the rat hippocampal slice preparation.","volume":"240","author":"Schurr","year":"1988"},{"key":"b36","series-title":"Glia","doi-asserted-by":"publisher","first-page":"56","DOI":"10.1002\/(SICI)1098-1136(19990101)25:1<56::AID-GLIA6>3.0.CO;2-4","article-title":"Glial swelling and astrogliosis produce diffusion barriers in the rat spinal cord.","volume":"25","author":"Sykova","year":"1999"},{"key":"b37","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"708","DOI":"10.3171\/jns.1981.55.5.0708","article-title":"Changes in extracellular potassium concentration in cortex and brain stem during the acute phase in experimental closed head injury.","volume":"55","author":"Takahashi","year":"1981"},{"key":"b38","series-title":"Am J Neurophysiol","doi-asserted-by":"publisher","first-page":"632","DOI":"10.1152\/jn.1997.77.2.632","article-title":"Inhibition of the electrogenic Na pump underlies delayed depolarization of cortical neurons after mechanical injury or glutamate.","volume":"77","author":"Tavalin","year":"1997"},{"key":"b39","series-title":"Lancet","first-page":"81","article-title":"Assessment of coma and impaired consciousness. A practical scale.","volume":"2","author":"Teasdale","year":"1974"},{"key":"b40","series-title":"J Neurosci","doi-asserted-by":"publisher","first-page":"877","DOI":"10.1523\/JNEUROSCI.16-03-00877.1996","article-title":"Metabolic coupling between glia and neurons.","volume":"16","author":"Tsacopoulos","year":"1996"},{"key":"b41","series-title":"J Neurotrauma","doi-asserted-by":"publisher","first-page":"509","DOI":"10.1089\/neu.1998.15.509","article-title":"Comparison of brain tissue oxygen tension to microdialysis-based measures of cerebral ischemia in fatally head injured patients.","volume":"15","author":"Valadka","year":"1998"},{"key":"b42","series-title":"Neurol Res","doi-asserted-by":"publisher","first-page":"334","DOI":"10.1080\/01616412.1997.11740821","article-title":"Mitochondrial dysfunction after experimental and human brain injury and its possible reversal with a selective N-type calcium channel antagonist (SNX-111).","volume":"19","author":"Verweij","year":"1997"},{"key":"b43","series-title":"J Neurophysiol","doi-asserted-by":"publisher","first-page":"1089","DOI":"10.1152\/jn.1990.63.5.1089","article-title":"Mechanism of potassium uptake in neuropile glial cells in the central nervous system of the leech.","volume":"63","author":"Wuttke","year":"1990"},{"key":"b44","series-title":"J Neurotrauma","doi-asserted-by":"publisher","first-page":"23","DOI":"10.1089\/neu.1997.14.23","article-title":"Mitochondrial dysfunction and calcium perturbation induced by traumatic brain injury.","volume":"14","author":"Xiong","year":"1997"},{"key":"b45","series-title":"Science","doi-asserted-by":"publisher","first-page":"1921","DOI":"10.1126\/science.274.5294.1921","article-title":"Reduction of voltage-dependent Mg2+ blockade of NMDA current in mechanically injured neurons.","volume":"274","author":"Zhang","year":"1996"}],"container-title":["Journal of Neurosurgery"],"original-title":[],"link":[{"URL":"https:\/\/thejns.org\/view\/journals\/j-neurosurg\/93\/5\/article-p800.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/thejns.org\/downloadpdf\/journals\/j-neurosurg\/93\/5\/article-p800.xml","content-type":"text\/html","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/thejns.org\/downloadpdf\/journals\/j-neurosurg\/93\/5\/article-p800.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,3,26]],"date-time":"2023-03-26T22:26:43Z","timestamp":1679869603000},"score":1,"resource":{"primary":{"URL":"https:\/\/thejns.org\/view\/journals\/j-neurosurg\/93\/5\/article-p800.xml"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2000,11]]},"references-count":45,"journal-issue":{"issue":"5"},"URL":"https:\/\/doi.org\/10.3171\/jns.2000.93.5.0800","relation":{},"ISSN":["0022-3085"],"issn-type":[{"value":"0022-3085","type":"print"}],"subject":[],"published":{"date-parts":[[2000,11]]}}}