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We challenged the current management of uncontrolled haemorrhagic shock (UHS) and put forward a hypothesis that therapeutic mild hypothermia combined with delayed fluid resuscitation will improve the survival rate. After an initial blood withdrawal of 3 ml/100 g for 15 min, the rat’s tail was amputated up to 75% to induce UHS phase I. The mean arterial blood pressure (MAP) was maintained at 40 mmHg or 80 mmHg, according to the assigned study group. This was followed by homeostasis of the tail wound and increase of the MAP up to 100 mmHg during resuscitation phase II. Finally, phase III was an observation of phase up to 72 h. Rats were anaesthetised and randomised into four groups. Group 1 received immediate fluid resuscitation and normothermia. Group 2 received immediate fluid resuscitation and therapeutic mild hypothermia. Group 3 received limited fluid solutions to maintain MAP at 40 mmHg and normothermia. Group 4 also received limited fluid solution, but the rats were subjected to therapeutic mild hypothermia. In groups 2 and 4, the body temperature was kept at 34 °C throughout the UHS phase I and resuscitation phase II. At the end of the observation phase III, the brains of the animals were fixed and analysed histologically. The blood loss from the tail during the UHS phase I was significantly higher in groups 1 and 2. The survival rate was 33.3, 83.3, 58.3 and 91.7%, respectively in groups 1–4. In all surviving rats, no histological brain damage was observed. These results indicate that therapeutic mild hypothermia or delayed fluid resuscitation increase the survival rate in this model. However, when mild hypothermia and limited fluid resuscitation were combined, the survival rate was the highest.

Study objective: we studied the long-term effect of a combined treatment with resuscitative mild hypothermia and induced hypertension on survival rate and neurological outcome after asphyxial cardiac arrest (CA) in rats. Methods: 36 male Wistar rats, were randomised into three groups: Group I (n = 10): anaesthetised with halothane and N2O/O-2 (70/30%) had vessel cannulation but no asphyxial CA; mechanical ventilation was continued to 1 h. Group II (n = 13). under the same anaesthetic conditions and vessel cannulation. was subjected to asphyxial CA of 8 min, reversed by brief external heart massage and followed by mechanical ventilation to 1 h post restoration of spontaneous circulation (ROSC). Group III (n = 13). received the same insult and resuscitation as described in group II, but in contrast to the previous group, a combination treatment of hypothermia (34 degreesC) and induced hypertension was started immediately after ROSC and maintained fur 60 min ROSC. Survival rate and neurological deficit (ND) scores were determined before arrest, at 3 and 24 h, and each 24-h up to 4 weeks after ROSC. Results: Baseline variables were the same in the three groups. Comparison of the asphyxial CA groups groups II and III), show ed an increased. although not statistically significant, survival rate at 72 h after ROSC in group III, and it became highly significant at 4 weeks after ROSC. The ND scores were the same in both asphyxial CA groups (groups II and III). Conclusions: Resuscitative mild hypothermia and induced hypertension after asphyxial CA in rats is associated with a better survival rate. This beneficial effect persisted for 4 weeks after ROSC. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

In het kader van de jaarlijkse wintermeeting van de Belgische Vereniging Gerontologie en Geriatrie van 2013 werden zes medicatiegroepen bij ouderen in woonzorgcentra tegen het licht gehouden. Voor de 80-jarigen en ouder moet individueel bekeken worden of het medisch gezien zinvol blijft om een farmacon voor te schrijven. Dit is afhankelijk van factoren zoals de comorbiditeit, de functionaliteit, de cognitie, de levenskwaliteit, de prognose, de bijwerkingen en de interacties. Het gebruik van statinen op hogere leeftijd staat ter discussie. Het nut van acetylcholinesteraseremmers in woonzorgcentra blijft vanuit wetenschappelijk standpunt en vanuit het oogpunt van de "evidence- based medicine" onzeker. Antistolling is even beschermend bij oudere patiënten met voorkamerfibrillatie (VKF) als bij jongeren, maar wordt onvoldoende gebruikt ("ageism"). In de groep kwetsbare ouderen in het woonzorgcentrum moet een antihypertensieve behandeling kritisch worden bekeken. Antidepressiva worden bij ouderen vaker voorgeschreven dan op grond van de epidemiologie van een majeure depressie verwacht zou worden. Antidepressiva hebben enkel een bewezen effect bij een majeure depressie. Protonpompremmers (PPI's) zijn in hun werking superieur aan de H2-antagonisten. Wie uitzonderlijk niet-steroïde anti-inflammatoire geneesmiddelen (NSAID's) opstart bij ouderen, moet ook steeds een PPI voorschrijven. De aanbevolen duur van de toediening bij reflux bedraagt vier tot acht weken. Er zijn gegevens nodig over het effect van deze medicatiegroepen bij 80-plussers. Een individuele aanpak met het afwegen van de voor- en de nadelen blijft in deze groep onder andere door een gebrek aan harde bewijzen moeilijk, maar aangewezen.

Resumen A pesar de los recientes avances en el tratamiento de los trastornos cardiovasculares en general y de las arritmias en particular, la muerte subita cardiaca continua siendo tanto un problema para el medico como un tema de salud publica de gran relevancia. Se estima que la incidencia anual de muerte subita cardiaca en todo el mundo oscila entre 4 y 5 millones de casos al ano. La informacion disponible sobre las causas y los mecanismos del sindrome de muerte subita cardiaca revelan que para reducirla sera necesario desarrollar nuevos y multiples enfoques, entre ellos tecnicas epidemiologicas para abordar las caracteristicas de riesgo especificas, la caracterizacion de los sucesos desencadenantes y la identificacion de personas concretas con riesgo de responder mal a estos sucesos, asi como metodos adecuados para evaluar la evolucion clinica tras un episodio de muerte subita cardiaca.

Bilateral interruption of the upper dorsal sympathetic chain at the D2 and D3 level represents the only permanent cure for essential hyperhidrosis. Following surgical sympathectomy, significant and symptomatic changes in pulmonary function have been observed. Since functional effects of the surgical intervention cannot be excluded, we wondered whether such alterations also occurred after thoracoscopic sympathicolysis; these should then be attributable to the surgical denervation itself. Pulmonary function tests (PFTs), including spirometry and body plethysmographic measurement of lung volumes and airway resistance and conductance, were compared before and 6 weeks after thoracoscopic sympathicolysis in 47 patients. In order to virtually exclude any effects of thoracoscopy on the test results PFTs were repeated 6 months after thoracoscopic sympathicolysis in 35 patients. Essential hyperhidrosis was completely relieved in all patients, thereby confirming the interruption of the D2-D3 sympathetic chain. None of the patients developed respiratory symptoms after thoracoscopic sympathicolysis. Forced expiratory volume in one second (FEV1) (-3%), forced expiratory flow after exhaling 75% of vital capacity (FEF75) (-8%) and total lung capacity (TLC) (-3%) were slightly but significantly reduced at six weeks after thoracoscopic sympathicolysis; whereas airway resistance (Raw) had increased (+12%). After correction for the small decrease in lung volume (FEV1/forced vital capacity (FVC), specific airway resistance (sRaw), specific airway conductance (sGaw))significant changes in "volume-dependent" PFT parameters were no longer observed. Smoking status had no influence on the reduction in FEF75. At 6 months after thoracoscopic sympathicolysis, TLC had returned to preoperative values, whereas FEF75 remained decreased (-8.6%). The decrease in airway calibre was confirmed by small but significant changes in FEV1/FVC (-2%) and Raw (+29%). We conclude that thoracoscopic sympathicolysis in patients with essential hyperhidrosis causes only minimal and subclinical changes in pulmonary function secondary to a temporary small decrease in lung volume, which in turn is probably inherent to the thoracoscopic procedure. D2-D3 sympathicolysis, in itself, is responsible only for a small and permanent decrease in forced expiratory flow, which suggests that, at least in essential hyperhidrosis patients, airway bronchomotor tone is influenced by sympathetic innervation.

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Background: Atypical haemolytic uraemic syndrome (aHUS) results from uncontrolled complement system activation. Complement factor H gene mutations are common causes of aHUS. Plasmatherapy, including plasma infusions and/or plasma exchanges, has been tried in this Setting with various successes. At present, we lack a specific marker to monitor functional factor H deficiency-related aHUS. Methods: We report the use of factor H functional assay in three patients-with atypical haemolytic uraemic syndrome. This assay is based on the requirement of soluble complement regulators that bind sheep red cells to prevent haemolysis. As factor H is highly abundant in the plasma, its defect results in haemolysis. Factor H activity was also measured among plasma donors. Results: One patient suffered from a plasma-dependent form of atypical haemolytic uraemic,syndrome, Plasma exchanges restored higher factor H activity-and were associated With a 15-months-disease-free period. In the two other patient, one With-a failingrenal graft and the-other-on chronic dialysis,,a bout of thrombotic micro-angiopathy was preceded by a drop of haemolytic activity below normal values. Plasma from healthy donors (N = 65) showed only minimal variations of Factor H activity (mean activity: 98.3%, SD=4.0). Conclusion: These preliminary data suggest that factor H activity could be of interest in both the diagnosis and the treatment by plasmatherapy of factor H-related aHUS.

Een beroerte of cerebrovasculair accident (CVA) wordt omschreven als een snel verlies van hersenfunctie ten gevolge van een stoornis in de bloedvoorziening van de hersenen. Hierbij kan het gaan om een herseninfarct of een hersenbloeding. Een herseninfarct komt frequenter voor dan een hersenbloeding en ontstaat meestal door een verstopping van een bloedvat door een bloedstolsel. Wegens een gebrek aan zuurstof en voeding (ischemie) kan het hersenweefsel achter de blokkade niet meer normaal functioneren waardoor snel onomkeerbare hersenbeschadiging zal ontstaan. Bij een hersenbloeding doet zich een scheurtje in een bloedvat voor, ...

Contexte: Les infections urinaires sont les infections les plus fréquentes chez le sujet âgé et la première cause de bactériémie. Une complication peu connue est l'hyperammoniémie liée à la présence d'une souche bactérienne uréase positive. Cette enzyme catalyse la réaction de transformation de l'urée en dioxyde de carbone et ammoniac. C'est surtout lors d'un épisode de rétention urinaire que l'infection se compliquera d'une absorption de l'ammoniac à travers une paroi vésicale étendue et amincie aboutissant à 'hyperammoniémie. Ceci peut alors être la cause d'une encéphalopathie avec confusion et altération de la conscience et nécessite un traitement spécifique rapide en plus du sondage et du traitement de l'infection urinaire. Observation: Une patiente âgée de 78 ans a été admise dans notre service pour dégradation de l'état général et altération de la conscience. Ses ATCD consistent en une démence à corps de Lewy traitée par rivastigmine patch et levo-dopa, une oesophagite de reflux sous omeprazole, une insuffisance cardiaque et VKF sous beta-bloquant et Aspirine, une osteoporose traitée par alendronate, vit. D et calcium, une colite d'origine incertaine traitée par mesalazine, une vessie hyperactive traitée par oxybutinine patch et des infections urinaires récidivantes. Par ailleurs la patiente reçoit des suppléments de vitamine B12, B6, acide folique et fer. Clinique: L'examen clinique montre une patiente mutique et difficilement éveillable avec un tremblement de la tête et un signe de Babinski bilatéral. Il n'y a pas de signes méningés. L'auscultation montre quelques râles crépitants aux deux bases pulmonaires et un rythme cardiaque irrégulièrement irrégulier. L'abdomen est distendu, mais dépressible et sensible au niveau sus-pubien, il n'y a pas de globe. Il n'y a pas d'oedème, ni signe de thrombose veineuze profonde aux membres. L'arrêt de l'oxybutinine n'améliore pas le tableau neurologique. Examens biologiques: La biologie met en évidence une fonction rénale N, Na 147mEq/L, K 3.4mEq/L. HCO3- et acide lactique N. Ca, P et Mg N. Il existe une légère élévation des LDH, ALP et de la bilirubine totale, sans élévation des transaminases. L'examen hematologique est normal. La CRP est normale. La TSH est à 5.15mUI/L (normalisée au controle). L'acide folique et la vitamine B12 sont élevés. Les gaz sanguins révèlent une pO2 à 86mmHg et une saturation à 96%. La culture urinaire met en évidence >100 000colonies de Klebsiella pneumoniae. L'ECG montre une FA avec réponse ventriculaire à +/- 90bpm. La radiographie de thorax ne met pas en évidence de foyer. Sur CT et RMN cérébrales, il existe une atrophie cortico-sous-corticale et une leucoencéphalopathie ischémique, mais pas d'accident vasculaire cérébral (AVC) aigu. L'EEG montre un ralentissement diffus en faveur d'une affection métabolique, mais pas de foyer irritatif. Une ammoniémie est prélevée sur avis du neurologue et s'élève à 113µg/dL en veineux et à 109µg/dL en artériel (N: 20-60). Diagnostic et traitement: On conclut à une hyperammoniémie sur infection urinaire et la patiente est traitée par Ciproxine et Duphalac avec une nette amélioration de sa conscience et un retour à son état mental antérieur. L'ammoniémie se corrige. Néanmoins un bilan hépatique par CT est demandé vu l'absence de syndrome inflammatoire et de rétention urinaire qui font douter du diagnostic initialement retenu. Un shunt porto-cave congénital est révélé et un controle ultérieur de l'ammoniémie montre à nouveau des valeurs légèrement élevées. Conclusion: L'origine pluri-factorielle des états confusionnels aigus reste un challenge et l'hyperammoniémie doit être envisagée même en l'absence de pathologie hépatique. L'hyperammoniémie de notre patiente résultait probablement de la combinaison de la bactériurie à Klebsiella, bactérie connue pour produire de l'uréase, et du shunt porto-cave congénital rare et révélé de façon exceptionnelle à cet âge.

Les résultats et facteurs de risque ont été analysés au sein d'une cohorte de 1.380 greffes rénales traitées par un inhibiteur de la calcineurine de 1983 à 2008 à l'Hôpital Erasme. Trois groupes correspondant à des périodes successives ont été comparés : A, de 1983 à 1992 (n = 463) ; B, de 1993 à 2000 (n = 470) ; C, de 2001 à 2008 (n = 447). Stable durant les périodes A et B, la survie du patient a diminué durant la période C (89 vs 85 % à 8 ans, P = 0,044) ; cet effet est principalement lié à l'âge des patients. En revanche, la survie du greffon a augmenté graduellement (64, 76 et 81 % à 8 ans pour les périodes A, B et C respectivement, P

Besides the classic "renal crisis", a well known form of acute renal failure sometimes complicating scleroderma, another type of acute renal injury, even rarer and not well recognized, does exist: a crescentic glomerulonephritis associated with ANCA, and more seldom with anti-GBM antibodies, which is often (but not always) secondary to the use of D-penicillamine. We report the case of a 70 years-old female who presented with a severe acute renal failure accompanied by positive anti-MPO ANCA as well as anti-GBM antibodies. She had a long history of systemic scleroderma which had been treated with D-penicillamine for many years. The clinical picture was typical of an ANCA-positive vasculitis of the microscopic form of polyangeitis, with a crescentic glomerulonephritis on renal biopsy. Unfortunately, the patient died despite therapy with plasma exchanges and immunosuppressive drugs. Some forty cases of crescentic glomerulonephritis associated with scleroderma have been reported. They were initially considered as always associated with D-penicillamine use, but more recently some observations have been made outside this drug context. As will be shown through a literature review, it can be concluded that there are two (or even three according to some authors) forms of acute renal involvement associated to scleroderma, which should be distinguished as soon as possible, given the quite differing therapeutic and prognostic consequences of this distinction.

Type 1 diabetes is caused by an immune mediated destruction of the insulin-secreting beta cells in the pancreas. The disease can become clinically apparent at any age. At clinical diagnosis, there is invariably some residual beta cell function. Recent studies--including one mainly conducted in Belgium--have provided proof of principle that short-term humanized anti-T-cell antibody treatment is able to preserve residual beta cell function for at least 18 months in adult type 1 diabetic patients with a recent clinical onset of disease. The effect of anti-T-cell antibody treatment is more pronounced among patients with initial higher residual beta-cell function. The resultant stabilizing effect on metabolic control is expected to delay chronic complications and avoid hypoglycemia in these patients. With a similar goal in mind, non-uremic C-peptide negative type 1 diabetic patients are offered beta cell transplantation. During the last years the one year survival of these grafts under immune suppression with Anti-Thymocyte-Globulin, tacrolimus and mycophenolate mofetil exceeds 80% with virtually no cases of primary non-function. Widespread application will however only occur if ways are found to induce operational graft tolerance and the shortage of viable human donor cells can be overcome. Both islet xenotransplantation and stem cell therapy provide possible strategies to solve this problem and represent areas of intense investigation. The ultimate goal is prevention of clinical disease. Studies by the Belgian Diabetes Registry and others in first degree family members of type 1 diabetic patients have refined identification of individuals at very high risk of hyperglycemia so that new immunological treatments can be tested in the prediabetic phase.

Background. Older and marginal donors, increasingly used to overcome organ shortness, often have a cerebrovascular accident as cause of death and could have vascular lesions in their kidneys. Methods. In this literature study, we evaluated the predictive value of vasculopathy in the renal allograft at the time of transplantation, on the subsequent graft function. Results. Short-term graft survival rates do not seem to be diminished by suboptimal donor histology. When vasculopathy is clearly present at the time of transplantation, impaired kidney function is showed at 1-week posttransplantation, at hospital discharge, or at 3 months and an increased frequency of delayed graft function. The long-term graft survival rate, in the studies of Pokorna and Taub, was significantly lower in the group with arteriolosclerosis. Wang et al. concluded in their study that arterial fibrous intimal thickening is the single most important histological predictor of both graft loss and delayed graft function. However, Minakawa et al. observed no significant correlation between 1 or 2-year graft survival and vasculopathy score. Severe vascular lesions in the donor kidney do affect the level of kidney function in the later posttransplant period as described in different studies (follow-up till 7 years posttransplantation). Conclusions. Data obtained from the studies of donor biopsies sustain the notion that vasculopathy is a major determinant of the short-term and the long-term outcome of the kidney allograft.

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Certain surgical techniques may improve pulmonary function, exercise capacity and quality of life in selected patients suffering from severe end-stage emphysema, who remain symptomatic despite maximal pharmacological and non-pharmacological treatment. Bullectomy can be offered to patients with a giant bulla; lung volume reduction surgery can be proposed to patients with severe but not catastrophic, heterogeneous emphysema; and lung transplantation may constitute an option in relatively young patients with end-stage, homogeneous emphysema associated with hypoxemia, hypercapnia and pulmonary hypertension. As lung volume reduction surgery is associated with significant morbidity and mortality, less invasive alternative treatments are currently being investigated. Recently, various bronchoscopic techniques have been developed. Intrabronchial placement of one-way valves in patients with heterogeneous emphysema, as well as the creation of extra-anatomical airways by means of bronchial perforation followed by placement of drug-eluting stents seem the most promising.

Objective: We investigated whether serum levels of neuron-specific enolase (NSE) and S-100β protein could be used to evaluate cerebral injury and to predict outcome in severe sepsis and severe septic shock. Design: Prospective study. Setting: University hospital. Patients and Measurements: In 170 consecutively enrolled patients with severe sepsis and septic shock, serum S-100β and NSE were measured daily during four consecutive days after intensive care unit admission. Admission Glasgow Coma Scale before sedation and daily Sequential Organ Failure Assessment scores were recorded in all patients. Acute encephalopathy was defined as either a state of agitation, confusion, irritability, and convulsions (type A) or characterized by somnolence, stupor, and coma (type B) and persistently observed during 72 hrs after withdrawing sedation. When clinically indicated, contrast computed tomography or magnetic resonance imaging were performed to evaluate brain injury. Main Results: S-100β and NSE increased in, respectively, 72 (42%) and 90 (53%) patients. High biomarker levels were associated with the maximum Sequential Organ Failure Assessment scores (p = .001), and the highest values were found in patients who died early, within 4 days of inclusion (p = .005). Low consciousness encephalopathy type B was more frequently observed in patients with elevated S-100β (p = .004). S-100β levels of ≥4 μg/L were associated with severe brain ischemia or hemorrhage, and values of

Wireless video-endoscopy of the small bowel is a relatively new diagnostic tool with only limited paediatric experience. We report our observations in 2 children. The capsule was easily swallowed and passed uneventful through the digestive tract of a child with unexplained anaemia not older than 5 years, although the literature mentions 10 years as minimal age. In a second child, 8 years old, with recurrent episodes of acute abdominal pain, the capsule confirmed an ileo-ileal intussusception. The absence of any exposure to radiation and the non-invasive character of this technique render it of extreme interest for paediatric use. Unfortunately, the Belgian social security does not yet reimburse it. Further investigations will be needed to evaluate if video-endoscopy may replace contrast radiological examinations in children with unexplained small bowel disease.

Resuscitative mild hypothermia is and will increasingly be used in the emergency department as protection for the brain after an ischaemic insult. The clinical application of resuscitative mild hypothermia and its limitations will be summarized in this paper. The evidence for each application and its underlying mechanism will also be reviewed.

Objective: To test the hypothesis that resuscitative mild hypothermia (MH) (34 degrees C) or breathing fractional inspired oxygen (FIo(2)) of 1.0 would prolong survival time during lethal uncontrolled haemorrhagic shock (UHS) in mechanically ventilated rats. Methods: Forty Wistar rats were anaesthetized with halothane, nitrous oxide and oxygen (70/30%), intubated and mechanically ventilated. UHS was induced by volume-controlled blood withdrawal of 3 ml/100 g over 15 min, followed by 75% tail amputation of its length. The animals were randomly divided into four UHS treatment groups (10 rats in each group): group 1 was maintained on an FIo(2) of 0.21 and rectal temperature of 37.5 degrees C. Group 2 was maintained on an FIo(2) of 0.21 and induced MH. Group 3 was maintained on an FIo(2) of 1.0 and 37.5 degrees C. Group 4 was maintained on an FIo(2) of 1.0 and MH. Rats were observed otherwise untreated until death. Results: During the initial blood withdrawal, mean arterial pressure (MAP) decreased to 40 mmHg, and the heart rate (HR) increased up to 400 beats/min. The induction of MH increased MAP to 60mmHg and increased survival time. Moreover, it reduced the HR to 300 beats/min but did not increase bleeding. Ventilation with an FIo(2) of 1.0 did not influence MAP, blood loss or survival time, but increased arterial oxygen tension. The mean survival time was 62, 202, 68 and 209 min in groups 1, 2, 3 and 4, respectively. Blood loss from the tail was 1.0, 1.2, 0.9 and 0.7 ml, respectively, in groups 1, 2, 3 and 4. Conclusion: MH prolonged the survival time during UHS in mechanically ventilated rats. However, an FIo(2) of 1.0 did not influence the survival time or blood loss from the tail. (C) 2004 Lippincott Williams & Wilkins.

The incidence of severe sepsis and septic shock is increasing and its mortality remains unacceptably high. A new definition and classification of sepsis aims at better patient identification and guidance of therapeutic approach. Many randomised studies during the last few years have demonstrated an important decrease of mortality with the use of new treatment strategies. Rigorous preservation of normoglycemia in ICU-patients is a preventive strategy. In a population of predominantly cardiosurgical patients this approach provokes a spectacular decrease of bacteremia and mortality. Another study evaluates the effect of more intensive resuscitation during the first 6 hours of treatment of severe sepsis and septic shock. Early "hard" target values for a number of vital and monitoring parameters result in a significant decrease of 28-day mortality. Relative adrenal insufficiency does occur in a large number of septic shock patients. Substitution of low-dose corticosteroids causes a significant decrease of mortality. Lung-protective ventilation using low tidal volumes lowers the mortality of the "Acute Respiratory Distress Syndrome" ("ARDS") that affects many patients with severe sepsis. Finally, adjuvant therapy with recombinant human activated protein C (drotrecogin alfa activated) beneficially influences survival of severe sepsis. The administration of hypertonic fluids, the use of vasopressin (analogues) in noradrenaline-resistant septic shock and continuous and "high volume" hemofiltration are promising therapeutic options of however still unproven benefit.

The present study investigated whether postischemic mild hypothermia attenuates the ischemia-induced striatal glutamate (GLU) and dopamine (DA) release, as well as astroglial cell proliferation in the brain. Anesthetized rats were exposed to 8 min of asphyxiation, including 5 min of cardiac arrest. The cardiac arrest was reversed to restoration of spontaneous circulation (ROSC), by brief external heart massage and ventilation within a period of 2 min. After the insult and during reperfusion, the extracellular glutamate and dopamine overflow increased to, respectively, 3000% and 5000% compared with the baseline values in the normothermic group and resulted in brain damage, ischemic neurons and gliosis. However, when hypothermia was induced for a period of 60 min after the insult and restoration of spontaneous circulation, the glutamate and dopamine overflows were not significantly different from that in the sham group. Histological analysis of the brain showed that postischemic mild hypothermia reduced brain damage, ischemic neurons, as well as astroglial cell proliferation. Thus, postischemic mild hypothermia reduces the excitotoxic process, brain damage, as well as astroglial cell proliferation during reperfusion. Moreover, these results emphasize the trigger effect of dopamine on the excitotoxic pathway. (C) 2004 Elsevier B.V. All rights reserved.

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