Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Barbiturates reduce cerebral activity which again reduce the cerebral metabolic rate probably by activating chloride channels and potentiating GABA's effects on these channels. Protection of the brain against hypoxia might theoretically occur by this mechanism, by vasoconstriction or by inhibiting calcium or glutamate. The barbiturates appear to have a positive effect in head-injury patients with high ICP uncontrollable by conventional therapy (in one study 5% of patients with a GCS < or = 7), and in animal studies of regional ischemia. No effect has been established in complete cerebral ischemia (cardiac arrest). The barbiturates have a depressant effect on the cardiovascular and respiratory systems, and the patients require intensive care. Thus there are some indications in the literature that the barbiturate treatment itself causes complications, and it is possible that this might cancel a potential beneficial effect in some patients. Clinically, the barbiturates are effective anticonvulsants, can be used in an attempt to control an elevated ICP uncontrollable by conventional means, and during transient ischemic episodes in the operating room with adequate monitoring and support systems already in place.
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PMID:Barbiturates in neuroanesthesia and neuro-intensive care. 184 34

We believe that somatosensory and brainstem auditory evoked response studies help in the understanding of the dysfunction of the ascending sensory pathyways at various levels. In some patients where EEGs showed a significant contamination of muscle and background noise, the SEP studies helped to identify the level of dysfunction. The severity of the clinical condition (GCS score) correlated significantly (p = 0.003) with the prolongation of the CCT. Asymmetries in CCTs were more frequent in the stroke group than in the other groups. The presence of asymmetries in CCT in diffuse encephalopathies indicated a variable degree of dysfunction in the ascending sensory pathways, which clinically were not easily identifiable. This fact raised the possibility of either pre-existing lesion(s) or recent insult(s) such as ischemia. The presence or absence of N20 appeared to influence the duration of survival in subgroups. Some degree of difference in duration of survival was noted among the metabolic group with and without N20 potential. The subset of patients with N20 potential survived relatively longer than the group without it. A suggestion of influence was seen in the stroke group, but caution must be exercised because the absence of N20 was compatible with survival. The hypoxic group did not show any difference. A combination of prolonged interpeak EP-N13 and N13-N20 indicated a poor prognosis. A distinct absence of Wave I in BAER limited its usefulness on some occasions. A combination of abnormal interpeak III-V and abnormal CCT seemed to suggest a poor prognosis. Although death generally occurred earlier in the stroke group, age did not seem to influence the mortality in the first 10 days. Similarly, the cause of death also did not seem to influence the course in those 10 days. None of the adult patients survived.
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PMID:Somatosensory and brainstem auditory evoked potential studies in nontraumatic coma. 339 8

Non-protein thiols (NP-SH) and the activities of the glutathione status-regulating enzymes gamma-glutamylcysteine synthetase (G-GCS), gamma-glutamyl transpeptidase (G-GT) and glutathione reductase (GR) were assessed in perfused rabbit hearts subjected to severe (60 min) or mild (7 min) total ischemia and 30 min reperfusion. Severe ischemia significantly decreased NP-SH, which were further depressed on reperfusion together with a significant decline in G-GCS activity; G-GT and GR activities were unchanged. Specific analytes were unaffected by mild ischemia-reperfusion. Thus, impaired enzymatic biosynthesis of GSH is operative in the reperfused rabbit myocardium after 60 min ischemia. This phenomenon may favour myocardial GSH depression and oxidative reperfusion injury after severe ischemia.
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PMID:Impaired glutathione biosynthesis in the ischemic-reperfused rabbit myocardium. 870 34

The aim of the study was to find out whether there is a correlation between the tissue-pO2 (ti-pO2) measurement and the lactate-oxygen index (mLOI). Both methods are to be considered as methods to detect brain ischemia. We studied 7 patients after severe head injury (GCS < 8) with a jugular bulb catheter and a tissue pO2 probe. Possible ischemia was defined with ti-pO2 below 10 mm Hg and mLOI above 0.08. 67 pairs of ti-pO2 and corresponding mLOI were found. In 5 cases out of the 7 cases with a ti-pO2 below 10 we found a pathological mLOI above 0.08. In 11 cases with pathological mLOI values, however, we found only 6 cases of decreased ti-pO2. The absolute values did not correlate. The sensitivity to predict normal values is above 85% with both methods. The specifity to predict ischemia is low (< 72%). The reason is the fact, that ti-pO2 is a local method in contrast to the mLOI values. In cases of diffuse brain injury without major contusions there should be a correlation between ti-pO2 and the mLOI.
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PMID:Brain ischemia detected by tissue-PO2 measurement and the lactate-oxygen index in head injury. 977 75

Fifty-five head injured patients (GCS < 8) were studied at an average of 7.5 +/- 3.4 days on the ICU to check quality of hemodynamic monitoring and the consequences for therapy. Multimodal neuromonitoring included intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), endtidal CO2 (EtCO2) as well as brain tissue--pO2 (p(ti)O2), regional oxygen (rSO2) and jugular venous oxygen saturation (SjO2). Regional p(ti)O2 as well as global SjO2 were sensitive technologies to detect hemodynamic changes. However analyzing reliability and good data quality regional p(ti)O2 (up to 95%) was superior to jugular bulb oximetry (up to 50%). Longterm-measurements of rSO2 using near infrared spectroscopy reached, if possible, a restricted reliability (good data quality up to 70%) and sensitivity in comparison to p(ti)O2. Especially p(ti)O2 enabled detection of critical p(ti)O2 (< 15 mm Hg) in up to 50% frequency during the first days after trauma and a second peak after day 6 to 8 according to evidence of CPP insults. Knowledge of baseline p(ti)O2 and CO2-reactivity allowed minimizing risk of ischemia by induced hyperventilation and improvement on cerebral microcirculation after mannitol administration could be individually recognized.
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PMID:Multimodal hemodynamic neuromonitoring--quality and consequences for therapy of severely head injured patients. 977 1

We examined the metabolic response of the brain underlying subdural hematomas or surrounding contusions to hyperventilation and looked for evidence of ischemia. Twelve consecutive patients with severe traumatic brain injury (TBI) (GCS < 8) who required surgery for evacuation of subdural hematoma or hemorrhagic contusion were studied. At surgery, a microdialysis catheter was placed into the cortex in a gyrus adjacent to the contusion or underlying the subdural hematoma. A thermal diffusion flow probe was placed on the cortex directly above the dialysis catheter. On days 1 and 3 post injury, two trials of hyperventilation were performed which dropped the patients' pCO2 10 mm Hg for 30 minutes. Monitoring of CBF and collection of dialysis fluid continued throughout each hyperventilation trial. Data was analyzed for a three hour window surrounding each hyperventilation. Brief periods of hyperventilation did not cause a significant elevation of the extracellular lactate/pyruvate ratio or glutamate level in areas of the brain likely to be the most vulnerable to secondary injury. In spite of hyperventilation leading to a significant decline in local CBF in 20% of the trials, there was no evidence of ischemia or excitatory amino acid release associated with hyperventilation.
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PMID:Effect of hypocapnea on CBF and extracellular intermediates of secondary brain injury. 1063 76

Having determined that edema and not vascular engorgement is the major factor leading to traumatic brain swelling, the objective of this study was to determine which type of edema, cellular or vasogenic, is responsible for increased tissue water in patients with focal lesions. Severely head injured patients (GCS 8 or less) were transported to imaging suites for measurement of brain water and apparent diffusion coefficient (ADC) using magnetic resonance technique. Cerebral blood flow by stable Xenon method was also measured in the regions of interest. Brain water was increased significantly in the hemisphere with lesion. The increase in water was associated with reduced ADC signifying a predominant cellular edema. The ADC in the contralateral hemisphere was near normal value. Cerebral blood flow values in the regions of interest were above ischemic levels suggesting that factors other than ischemia are responsible for the cytotoxic swelling in patients with focal injury.
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PMID:Distinguishing between cellular and vasogenic edema in head injured patients with focal lesions using magnetic resonance imaging. 1145 41

Adrenomedullin is a recently discovered 52-amino-acid peptide that is a potent vasodilator. Infusion of adrenomedullin increases regional cerebral blood flow and reduces infarct volume after vascular occlusion in rats. Adrenomedullin may represent an endogenous neuroprotectant since it is increased after focal brain ischemia. Cerebral hypoperfusion is present after traumatic brain injury (TBI) in children. We hypothesized that adrenomedullin levels would be increased in children with severe TBI. Total adrenomedullin concentrations were measured using a radioimmunometric assay. Thirty-six samples of ventricular cerebrospinal fluid (CSF) from 10 pediatric patients were collected during the first 10 days after severe TBI (GCS < 8). Control CSF was obtained from 5 children undergoing lumbar puncture, who had normal CSF parameters and no evidence of central nervous system infection. Patients underwent standard neuro-intensive care, including cerebrospinal fluid drainage. Data were analyzed using a univariate regression model. Adrenomedullin concentration was markedly elevated in CSF of children following TBI versus control (mean level 10.65 vs 1.51 fmol/ml, p = 0.006). All 36 case samples had an adrenomedullin concentration above the median value for the controls (1.52 fmol/ml). We conclude adrenomedullin is elevated in the CSF of children following severe TBI. We speculate that it participates in the endogenous response to cerebral hypoperfusion after TBI.
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PMID:Increased adrenomedullin in cerebrospinal fluid after traumatic brain injury in children: a preliminary report. 1145 58

Traumatic brain contusions have been associated with regional ischemia. We aimed to measure the effect of induced supra-normal values of cerebral perfusion pressure (CPP) on regional cerebral blood flow (rCBF) in the intracontusional low density area surrounding the contusional hemorrhagic core. In 7 severely head injured patients (GCS < or = 8) harbouring a contusion larger than 2 cm, the rCBF levels were measured, by means of Xenon-enhanced CT, in: 1) the intracontusional low density area: 2) contralaterally, in a normal brain symmetric area. CBF studies were performed at a baseline CPP of 65.3 mmHg +/- 7 and after 20 minutes of norepinephrine-induced CPP supernormal values (88.3 mmHg +/- 10.5) (p = 0.0013). A "paradoxical" reduction of rCBF levels was observed in both the intracontusional low density area (p = 0.07) and the contralateral "normal" area (p = 0.08). In particular, this decrease of rCBF in the intracontusional low density area (-25.7 + 10 ml/100gr/min) (p = 0.0009) was present in only 4 cases, having a mean rCBF at baseline of 25 +/- 16 ml/100gr/min. In the remaining 3 cases in which rCBF at baseline was abnormally low (12 +/- 7 ml/ 100gr/min), rCBF values improved slightly (3.6 +/- 2 ml/100gr/min) (p = 0.61). An acute increase of CPP seems to marginally affect rCBF in the intracontusional low density area having critically reduced initial values, but may greatly reduce rCBF in subjects starting from non-critical baseline values.
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PMID:Induced acute arterial hypertension and regional cerebral flow in intracontusional low density area. 1475 69

Excitotoxicity and ischemia can result in oxidative stress after TBI. Female sex hormones are hypothesized to be neuroprotective after TBI by affecting multiple mechanisms of secondary injury, including oxidative damage, excitotoxicity and ischemia. Ca2+ mediated oxidative stress increases with age, and hypothermia is known to attenuate secondary injury. The purpose of this study was to determine if the relationship between cerebral spinal fluid (CSF) markers of excitotoxicity, ischemia, and oxidative damage are gender and age specific and the role of hypothermia in affecting these relationships. F2-isoprostane, glutamate, and lactate/pyruvate, were assessed in CSF from adults (n = 68) with severe TBI (Glasgow coma scale [GCS] score </= 8) using ventricular CSF samples (n = 207) collected on days 1, 2, and 3 post-injury. F2-isoprostane/glutamate and F2-isoprostane/lactate/pyruvate ratios were determined for patients at each time point. Six-month Glasgow Outcome Scores (GOS) were also obtained. Repeated measures multivariate analysis showed a significant gender effect (p < 0.002) and gender*time interaction (p = 0.012) on F2-isoprostane/glutamate ratios. A significant gender effect (p = 0.050) and gender*time interaction (p = 0.049) was also seen with F2-isoprostane/lactate/pyruvate. Hypothermia (p = 0.001) and age (p = 0.026) significantly increased F2-isoprostane/glutamate ratios. Females had a significant inverse relationship between day 1 F2-isoprostane/glutamate ratios and GOS scores (r =- 0.43; p = 0.05) as well as day 1 F2-isoprostane/lactate/pyruvate ratio (r =- 0.46; p = 0.04) and GOS scores. These results indicate that females have smaller oxidative damage loads than males for a given excitotoxic or ischemic insult and female gonadal hormones may play a role in mediating this neuroprotective effect. These results also suggest that susceptibility to glutamate mediated oxidative damage increases with age and that hypothermia differentially attenuates CSF glutamate versus F2-isoprostane production. Gender and age differences in TBI pathophysiology should be considered when conducting clinical trials in TBI.
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PMID:Relationships between cerebrospinal fluid markers of excitotoxicity, ischemia, and oxidative damage after severe TBI: the impact of gender, age, and hypothermia. 1500 Jul 54


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