Sustained elevation of cerebrospinal fluid glucose and lactate after a single seizure does not parallel with mitochondria energy production.

Generalized seizures trigger excessive neuronal firing that imposes large demands on the brain glucose/lactate availability and utilization, which synchronization requires an integral mitochondrial oxidative capability. We investigated whether a single convulsive crisis affects brain glucose/lactate availability and mitochondrial energy production. Adult male Wistar rats received a single injection of pentylentetrazol (PTZ, 60 mg/kg, i.p.) or saline. The cerebrospinal fluid (CSF) levels of glucose and lactate, mitochondrial respirometry, [14C]-2-deoxy-D-glucose uptake, glycogen content and cell viability in hippocampus were measured. CSF levels of glucose and lactate (mean ± SD) in control animals were 68.08 ± 11.62 mg/dL and 1.17 ± 0.32 mmol/L, respectively. Tonic-clonic seizures increased glucose levels at 10 min (96.25 ± 13.19) peaking at 60 min (113.03 ± 16.34) returning to control levels at 24 h (50.12 ± 12.81), while lactate increased at 10 min (3.23 ± 1.57) but returned to control levels at 360 min after seizures (1.58 ± 0.21). The hippocampal [14C]-2-deoxy-D-glucose uptake, glycogen content, and cell viability decreased up to 60 min after the seizures onset. Also, an uncoupling between mitochondrial oxygen consumption and ATP synthesis via FoF1-ATP synthase was observed at 10 min, 60 min and 24 h after seizures. In summary, after a convulsive seizure glucose and lactate levels immediately rise within the brain, however, considering the acute impact of this metabolic crisis, mitochondria are not able to increase energy production thereby affecting cell viability.

Peripheral nucleotide hydrolysis in rats submitted to a model of electroconvulsive therapy.

Electroconvulsive therapy (ECT) is an efficacious and safe method for the treatment of mood disorders. Its utilization is accompanied by a myriad of biochemical and cellular changes, which are far from fully understood. The present work investigates in rat serum the effects of seizures induced by electroconvulsive shocks (ECS), an animal model of ECT, on enzymes that hydrolyze ATP, ADP and AMP to adenosine. Two different models of ECS were used, consisting in the application of one or eight ECS sessions, and respectively named acute or chronic. Serum samples were collected at several time points after the single shock in the acute and after the eighth and last shock in the chronic model. A single shock produced a sudden and short-lived inhibition of enzymatic activity (P<0.01 for ADP and AMP), whereas in the chronic model significant increases were noticed starting as early as 12 h after the last shock, remaining significantly elevated until the last measurement 7 days later for ATP and ADP. Analysis of hydrolysis was assessed at the selected time point of 7 days in cerebrospinal fluid samples, also demonstrating a significant activation in the chronic model (P<0.0001 for ATP and ADP). These results support the idea that adenosine nucleotides may be involved in the biochemical mechanisms underlying longer lasting therapeutic effects associated with ECT, and suggest that peripheral markers can possibly contribute to the evaluation of activity in the central nervous system.

Acute and chronic electroconvulsive shock in rats: effects on peripheral markers of neuronal injury and glial activity.

Electroconvulsive therapy is considered one of the most effective treatments of major depression, but controversy still exists on whether it may be brain damaging. The aim of this work was to evaluate the cerebrospinal fluid (CSF) levels of neuron specific enolase (NSE), protein S100B and lactate of rats submitted to acute and chronic models of ECS. Rats were submitted to either one shock (acute) or a series of eight shocks, applied one at every 48 h (chronic). CSF samples were collected at 0, 3, 6, 12, 24, 48 and 72 h after the shock in the acute model and at these same time intervals after the last shock in the chronic model. Both models did not produce significant alterations in the levels of NSE. S100B levels were significantly increased at 6 h in the chronic model (p<0.0001). There was a significant increase in the levels of lactate at 0 h in both models (p<0.001). These results support the proposition that ECS does not produce neural damage, and suggest that the alterations in the levels of S100B and lactate may reflect an astrocytic activity of a protective nature.

Resultados imediatos da eletrocoagulaçäo com argônio no tratamento do esôfago de Barrett em pacientes com e sem displasia / Endoscopic argon plasma coagulation (Beamer) of Barrett`s esophagus in patients with and without dysplasia

Intoduçäo e objetivo: O esôfago de Barrett (EB) é uma lesäo comprovadamente pré-maligna. As cirurgias anti-refluxo ou o tratamento farmacológico nem o revertem para epitélio escamoso, nem diminuem o risco de câncer associado a esta lesäo metaplásica. Recentemente, alguns estudos têm demonstrado reversäo do EB com diferentes técnicas endoscópicas associadas à inibiçäo ácida. Neste estudo os autores pretendem verificar se a reversäo completa do EB é possível através da APC. Métodos: foram tratados 32 pacientes -20M/12F, média etária =55,2 (21-84)- com EB demonstrado histologicamente com extensäo média de 3,9cm (0,5-6). Quatorze casos apresentavam displasia de baixo grau. Toda a extensäo do EB era cauterizada em cada sessäo usando o APC com uma potencia de 65-70W. Todos os pacientes recebiam 60mg de omeprazol durante o período de tratamento. Resultados: Reversäo completa do EB foi obtida em todos os pacientes após média de 1,9 sessäo (1-3). Esses resultados foram confirmados histologicamente por meio de múltiplas biópsias que evidenciaram epitélio escamoso. Dezessete (53por cento) pacientes sofreram dor retroesternal de forte a moderada intensidade com odinofagia por dois a dez dias após cada sessäo. Febre alta e derrame pleural ocorreram em cinco e estenose de esôfago em três desses 17 casos. Conclusäo: A eletrocoagulaçäo por argônio associada a supressäo ácida com omeprazol é um método efetivo em eliminar o EB, pelo menos, a curto prazo. Apenas estudos com seguimento a longo prazo desses pacientes, juntamente com alívio permanente do refluxo ( por cirurgia ou medicaçäo), poderäo determinar se essa técnica reduz ou elimina o risco de câncer associado ao EB

Erradicação do esofago de barrett através da eletrocoagulação por meio de argônio / Eradication of Barrett's esophagus with argon plasma coagulation

O esôfago de Barrett é uma alteração pré-maligna da mucosa do esôfago, que é caracterizada pela substituição do epitélio escamoso estratificado por epitélio cilíndrico simples do tipo gástrico, conjuntamente com a presença de metaplasia intestinal. As cirurgias anti-refluxo e os tratamentos medicamentosos não conseguiram demonstrar de forma consistente, em estudos prospectivos ou retrospectivos, que levam a regressão desse epitélio, nem que diminuem a probabilidade de sua transformação maligna. Recentemente a ablação por via endoscópica desse epitélio metaplásico tem sido realizada com sucesso por meio de laser, terapêutica fotodinâmica ou coagulação multipolar. Neste estudo, os autores relatam regressão completa do epitélio de Barrett em quatro pacientes após a aplicação por via endoscópica de eletrocoagulção por meio de argônio, conjuntamente com supressão ácida através de 60mg diários de omeprazol