Biomedical subjects

L L Guyot

Publications and source records attributed to L L Guyot.

13 recordsLinked to original sources

PubMed2001

Real-time measurement of glutamate release from the ischemic penumbra of the rat cerebral cortex using a focal middle cerebral artery occlusion model.

Following permanent middle cerebral artery occlusion, extracellular penumbral glutamate levels, measured by a real-time glutamate electrode, increased in two different patterns. In 7/11 rats, glutamate increased from baseline levels of 19+/-4 (mean+/-SEM) to 208+/-29 microM and then declined towards baseline levels. Blood flow in the penumbral area declined to 30% of pre-ischemic levels with recovery to 60 and 70% of baseline values by 3 and 6 h, respectively. Four of 11 rats in the study also exhibited late peaks of glutamate release (120+/-40 microM ) 2 h after the onset of ischemia. There were no changes in the EEG recordings or cerebral blood flow during these late glutamate peaks.

Animals↗

PubMed2001

The effect of streptozotocin-induced diabetes on the release of excitotoxic and other amino acids from the ischemic rat cerebral cortex.

OBJECTIVE: Hyperglycemic stroke results in increased neuronal damage, the exact mechanism of which is unknown. Lactic acidosis has been implicated; however, increases in the excitotoxic amino acid glutamate, which correlate with increased neuronal damage, may be the cause for the increased damage seen in hyperglycemic stroke. METHODS: Ten Sprague-Dawley rats were treated with streptozotocin (STZ; 50 mg/kg), and 12 normoglycemic rats were used as controls. Using a four-vessel occlusion model, global ischemia was assessed at 5 to 7 days after treatment in five animals (acute STZ group) or at 4 to 6 weeks after treatment in five animals (chronic STZ group). The cortical cup model was used to collect superfusates under basal, ischemic, and reperfusion conditions and analyzed for nine different amino acids using high-performance liquid chromatography. RESULTS: Plasma glucose levels were significantly higher in the acute and chronic STZ groups as compared with the control group. Plasma lactate levels were higher in the acute STZ group as compared with the control or chronic STZ groups. Extracellular cortical glutamate levels were significantly reduced during reperfusion in the acute STZ group and during ischemia/reperfusion in the chronic STZ group as compared with the controls. Levels of extracellular gamma-aminobutyric acid were significantly reduced in the acute and chronic STZ groups as compared with the controls. CONCLUSION: A chronic state of hyperglycemia results in reduction in extracellular brain glutamate levels during ischemia/reperfusion and therefore does not appear to be responsible for the increased neuronal damage seen in diabetic stroke. Chronic hyperglycemia also causes decreased extracellular gamma-aminobutyric acid levels, which, because of the loss of the inhibitory effects of this neurotransmitter, could contribute to the increased damage observed in hyperglycemic stroke.

Acute Disease↗

PubMed2000

The effect of topical insulin on the release of excitotoxic and other amino acids from the rat cerebral cortex during streptozotocin-induced hyperglycemic ischemia.

Insulin has been demonstrated to be neuroprotective in brain and spinal cord ischemia. The mechanism of neuroprotection may involve alterations in metabolism, protein synthesis or uptake of GABA by astrocytes. Conversely, hyperglycemia increases the extent of neurologic damage observed during ischemia/reperfusion. Diabetic patients are 2-4 times more likely to suffer a stroke as normoglycemic patients and they also have worsened neurologic outcome. Determining if insulin, which many diabetics already use as therapy, can be neuroprotective, would be a possible means of alleviating the detrimental outcome from diabetic stroke. This study looked at the relationship between topically administered insulin (1 mIU insulin/ml and 100 mIU insulin/ml) during a four vessel occlusion model of global ischemia and the release of amino acids, especially glutamate, from the cortex in streptozotocin (STZ)-treated rats. The rats were utilized either 5-7 days (ASTZ) or 4-6 weeks (CSTZ) after a single STZ injection. In the ASTZ animals both doses of insulin increased the amount of the excitotoxic amino acids, aspartate and glutamate, released during reperfusion and the higher dose also increased the levels of taurine and GABA during reperfusion. In the CSTZ animals, both doses of insulin increased the amount of excitotoxic amino acids during reperfusion and the lower dose increased GABA levels released during reperfusion. The differences between the ACTZ and CSTZ animals may be due to metabolic differences in the utilization of glucose. Insulin may act as a neuroprotectant by increasing extracellular GABA resulting in neuroinhibition.

Administration, Topical↗

PubMed2000

The effect of intravenous insulin on accumulation of excitotoxic and other amino acids in the ischemic rat cerebral cortex.

Insulin has been reported to be neuroprotective during cerebral ischemia/reperfusion. However, it may also increase the sensitivity of cultured cortical neurons to glutamate toxicity. The experiments described here utilized a rat four-vessel occlusion model with cerebral cortical windows to determine the effects of intravenous insulin, alone (I) or combined with glucose (IG) to maintain physiologic blood glucose levels, on the extracellular accumulation of amino acids in superfusates of the cerebral cortex. Aspartate, phosphoethanolamine, taurine and gamma-aminobutyric acid were increased in the I and IG groups and glutamate was increased in the IG group compared to controls during ischemia/reperfusion. Insulin treatment attenuated the rebound in cortical superfusate glucose levels in both groups of animals during reperfusion. The increases in amino acid release during reperfusion may be due to a lack of glycolytically derived energy available for amino acid uptake systems and ionic pumps.

Animals↗

PubMed2000

Topical insulin and accumulation of excitotoxic and other amino acids in ischemic rat cerebral cortex.

Insulin plays a neuroprotectant role in the brain and spinal cord during ischemia. However, studies have shown insulin to increase the sensitivity of cultured cortical cells to glutamate toxicity. The present study looked at the relationship between topically administered insulin (1 mIU insulin/ml and 100 mIU insulin/ml) during a four-vessel model of global ischemia and the accumulation of amino acids, especially glutamate, from the ischemic rat cerebral cortex. The lower dose of insulin was found to attenuate the release of excitotoxic and other amino acids from the cortex in ischemia/reperfusion. This may occur because insulin increases glucose availability to glial cells resulting in maintenance of glycolysis and ionic pumps that can reduce glutamate release and maintain uptake during ischemia/reperfusion. The higher dose of insulin, which significantly increased the amount of aspartate, glutamate, taurine, and GABA during reperfusion, may act to stimulate the amount of glycogen stored in astrocytes, reducing the availability of glucose for metabolic purposes.

Administration, Topical↗

PubMed2000

Topical glucose and accumulation of excitotoxic and other amino acids in ischemic cerebral cortex.

Pre-ischemic hyperglycemia aggravates brain damage due to transient global ischemia as demonstrated by exacerbation of brain lesions. Lactacidosis and elevated glutamate levels have been implicated as mechanisms of the increased damage. Our objective was to determine the effects of different levels of glucose (0, 66.5, 450 mg/dL) in cortical superfusates on the ischemia/reperfusion-evoked release of amino acids from the rat cerebral cortex. Physiologic levels of glucose significantly reduced the amount of aspartate, glutamate and gamma-aminobutyric acid and the supra-physiologic levels of glucose reduced the amount of aspartate and phosphoethanolamine released from the cortex during ischemia/reperfusion in comparison with no glucose. The decrease in glutamate release may be due to increased availability of glucose for glycolysis with the subsequent formation of ATP and lactate, which has been shown to act as an energy source for neurons. The decreased levels may also reflect the continued energy-dependent uptake of glutamate by glial cells.

Animals↗

PubMed2000

Post-traumatic hydrocephalus.

The syndrome of post-traumatic hydrocephalus (PTH) has been recognized since Dandy's report in 1914. The incidence of symptomatic PTH ranges from 0.7%-29%. If CT criteria of ventriculomegaly are used the incidence has been reported to be from 30%-86%. Differences in diagnostic criteria and classification have contributed to the variation in reported incidence. The diagnosis of PTH is established using a combination of clinical, imaging and physiologic data. Symptomatic PTH is to be distinguished from post-traumatic ventriculomegaly resulting from atrophy. Symptomatic PTH patients are likely to improve when treated by shunting. Ventriculomegaly secondary to atrophy is less likely to respond to shunting. A series of traumatic brain injury patients at Wayne State University has been followed since 1989. The overall incidence of shunt placement in this group is 3.65%. Future studies of PTH should be aimed at refining diagnostic classification and criteria. Analysis of a large PTH population may then identify alterable risk factors in the early post-traumatic brain injury period. Minimizing these factors will help prevent subsequent PTH and obviate the need for shunting.

Brain Injuries↗

PubMed2000

Adult rhombencephalosynapsis. Case report.

Rhombencephalosynapsis (RS) is a relatively rare developmental disorder of the cerebellum in which the cerebellar hemispheres are fused across the midline without being separated by a cleft or the vermis. The condition may be associated with hydrocephalus and other intracranial and extracranial abnormalities. The authors report on the case of a symptomatic adult who was successfully treated with suboccipital decompression and duraplasty. A 39-year-old woman presented with intractable pain radiating from the thoracolumbar column to the occiput. A general examination yielded normal findings and a neurological examination revealed only subtle ataxia of tandem gait. The patient underwent magnetic resonance (MR) imaging, the results of which revealed an absent cerebellar vermis with fusion of the cerebellum and mild hydrocephalus. A cine-MR image obtained to evaluate her cerebrospinal fluid flow (CSF) revealed attenuated flow in the posterior fossa and cerebral aqueduct. Preoperative intracranial pressure (ICP) monitoring demonstrated no elevation of ICP (mean 4.3 mm Hg). The patient consented to undergo suboccipital craniectomy and duraplasty. Despite an increase in postoperative ICP (mean 10.77 mm Hg; difference from preoperative level according to a t-test, p = 0.002), the patient experienced symptomatic relief, which has persisted for 3 years. One year postoperatively, a cine-MR image was obtained, which revealed improvement in the patient's CSF dynamics. The authors conclude that, although RS may cause altered flow in the adult, their patient has experienced symptomatic relief, suggesting that her pain was related to local pressure in the posterior fossa.

Adult↗

PubMed1999

Failure of kynurenic acid to inhibit amino acid release from the ischemic rat cerebral cortex.

The ability of a broad spectrum glutamatergic receptor antagonist, kynurenic acid (1 and 5 mM) to attenuate release of excitant and other amino acids from the ischemic cerebral cortex was examined in a four vessel occlusion rat model. Kynurenic acid, administered topically onto the cortex in artificial cerebrospinal fluid using bilateral cortical cups, failed to attenuate ischemia-evoked release of aspartate, glutamate, phosphoethanolamine, taurine and at 1 (but not 5) mM it depressed GABA release. There was no effect on basal, pre-ischemic, release. This result suggests that ischemia-evoked amino acid release is not a significant consequence of the activation of ionotropic receptors by synaptically released glutamate.

Amino Acids↗

PubMed1999

Lactate reduces amino acid release and fuels recovery of function in the ischemic brain.

Pre-ischemic hyperglycemia exacerbates the neuronal injury associated with cerebral ischemia/reperfusion, possibly because the accumulation of glycolytically derived lactate causes acidosis. Twenty minutes of four vessel occlusion caused significant increases in rat cerebral cortical superfusate levels of aspartate, glutamate, phosphoethanolamine, taurine, and GABA. Lactate (20 mM), applied topically, significantly reduced the ischemia/reperfusion evoked releases of glutamate and GABA, with further reductions following the higher dose (40 mM), which also significantly reduced the evoked release(s) of the other amino acids. EEG recovery was robust in the presence of 40 mM lactate. These results substantiate the ability of lactate to serve as a neuronal energy substrate but question the role of lactate accumulation in the enhancement of ischemic brain injury by hyperglycemia.

Amino Acids↗

PubMed1999

5-(N-Ethyl-N-isopropyl)-amiloride, an Na(+)-H(+) exchange inhibitor, protects gerbil hippocampal neurons from ischemic injury.

The effect of the selective Na(+)/H(+) antiporter inhibitor 5-(N-ethyl-N-isopropyl)-amiloride (EIPA) on cerebral ischemia/reperfusion injury was evaluated in the Mongolian gerbil. Ischemia was induced in unanaesthetized gerbils by a 5-min period of bilateral common carotid artery occlusion followed by reperfusion for 6 days. Two groups of gerbils were injected intraperitoneally with either dimethyl sulfoxide (DMSO; 10 microl) or EIPA (5 mg/kg in 10 microl DMSO) 30 min prior to ischemia. The increase in locomotor activity in the EIPA-treated group was significantly less than that of the control group at both 24 h and 6-day post-ischemia. The extent of CA1 pyramidal neuron loss was significantly reduced in the EIPA-treated group in comparison with that of DMSO treated controls. These results suggest that EIPA can protect cerebral neurons from ischemia/reperfusion injury and implicates acidosis and Na(+)/H(+) exchange as a causative factor in such injury.

Amiloride↗

PubMed1998

Cerebral monitoring devices: analysis of complications.

The use of indwelling cerebral monitoring devices (ICMDs) is common in the intensive care of neurosurgical patients. ICMDs are used to measure and treat intracranial pressure (ICP), temperature, blood flow and the microchemical environment. Intracranial hemorrhage (ICH) and infection are risks of ICMD use [4]. This study presents ICMD use at Detroit Receiving Hospital (DRH) from July 1993- March 1997. Analysis of complications associated with ICMD placement will test the hypothesis that complication rate depends upon type of ICMD used. A log of all patients having ICMDs at DRH has been kept since 1993. This log was used to identify complications of ICMD placement. Each case was reviewed and the following data obtained: diagnosis, patient age, initial Glasgow Coma Score, Glasgow Outcome Score, type of ICMD, number of ICMDs per patient, duration of implant and complication. Descriptive and non-parametric statistics were used to compare samples of interest. The following number of ICMDs were placed: 274 ventriculostomies, 229 Camino intra parenchymal ICP monitors, and 33 other ICMDs. Complications in these 536 cases include 21 infections, 15 ICHs, 1 granuloma and 1 persistent cerebrospinal fluid leak. Complication was analyzed as a function of ICMD type using Chi-Square test for independence. The rate of infection and ICH was significantly higher in the ventriculostomy group (p = 0.0001). These results support the hypothesis that complications of ICMD use are due to the type of device implanted. The determinants of ICMD complication is undoubtedly multifactorial. The clinician must consider the complication rate related to a particular ICMD among other factors when choosing to place an ICMD.

Brain Injuries↗

PubMedDate not supplied

Vascular injury in neurotrauma.

Traumatic vascular lesions can occur after severe or even the most mild of head and cervical trauma. The initial evaluation of the injured patient must be thorough and the clinical suspicion of vascular injury must be highly suspected based on the mechanism of injury. Traumatic vascular injuries can be broadly classified into traumatic aneurysms, dissections and occlusions and fistulae of the carotid or vertebral arteries. The current management and treatment options of each condition are discussed.

Brain Injuries↗