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1.
Korean Journal of Anatomy ; : 225-234, 2009.
Artigo em Coreano | WPRIM | ID: wpr-653625

RESUMO

Ischemic preconditioning is the earlier stress adaptive response that occurs during repeated episodes of the brief ischemia and reperfusion. It is now well known that this adaptive response can render the neuron more tolerant to the subsequent potential lethal ischemic injury. Although the selective mitochondrial K+ (ATP) channel opener induces protective effects similar to that of ischemic preconditioning, the underlying mechanism is not known yet. The purpose of this study was to investigate the mechanism of neuroprotective effect of diazoxide, a mitochondrial K+ (ATP) channel opener, pretreatment on a focal cerebral ischemic injury of rat brain. Thirthy-four Sprague-Dawley rats were used. Animals were randomly divided into normal control group, middle cerebral artery (MCA) permanent occulusion group (experimental control group), and diazoxide pretreated group. Animals were sacrified at 2 hours or 24 hours after MCA occulusion injury. For inducing the focal cerebral ischemic injury, the left MCA was occuluded by modified Longa's method. Diazoxide (3 mg/kg) was administrated through the femoral artery at 15 minutes earlier to surgical procedures. TTC-stained brain sections of experimental group showed a remarkable infarct injury in the ipsilateral cerebral cortex and striatum. However, the infarction volume of the diazoxide pretreated group was significantly reduced. Accordingly, the number of neurons undergoing eosinophilic degeneration and nuclear chromatin condensation was reduced by diazoxide pretreatment. TUNEL-positive neurons were not detected at 2 hours after MCA permanent occlusion but lots of them were observed at 24 hours. The number of c-fos immunoreactive neurons was remarkably increased at 2 hours following MCA permanent occulusion and reduced to the basal level at 24 hours in both experimental control and diazoxide pretreated group. However, the number of Bcl-2 or pAkt immunoreactivitive neurons of the diazoxide pretreated group outnumbered those of the experimental control group at all timepoints in our experiment. In conclusion, the pretreatment of diazoxide, K+ channel opener, could have europrotective effects on ischemic neurons by upregulating the expression of anti-apoptotic proteins, like Bcl-2 or pAkt.


Assuntos
Animais , Ratos , Apoptose , Proteínas Reguladoras de Apoptose , Encéfalo , Isquemia Encefálica , Córtex Cerebral , Cromatina , Diazóxido , Eosinófilos , Artéria Femoral , Infarto , Isquemia , Precondicionamento Isquêmico , Artéria Cerebral Média , Modelos Animais , Neurônios , Fármacos Neuroprotetores , Ratos Sprague-Dawley , Reperfusão
2.
Journal of the Korean Neurological Association ; : 158-163, 1995.
Artigo em Coreano | WPRIM | ID: wpr-121830

RESUMO

We have had an opportunity to study a patient with acute sensory neuronopathy. The patient was a 32-yearold housewife; the rapidly spreaded tingling sensation along both arms and legs developed, rendering her severely ataxic. There was no history of antecedent illness, familial neurological disease, or exposure to toxins and special drugs. On examinations, there was no abnormality in her mental and cranial nerve function. There was no motor weakness. She showed the profound loss of kinesthetic sense which was acutely progressive and associated with severe sensory ataxia and pseudoathetosis. All tendon reflexes were absent. However, cutaneous senses were preserved. There was no significant abnormal laboratory finding except elevated CSF protein content. On electrophysiologic findings, the decrease in the amplitude of action potentials with only mild slowing of conduction velocities of sensory nerves were found even though motor nerve conduction studies were normal. Median and tibial somatosensory evoked potentials could be elicited, although the median N19 scalp response and tibial N45 waveforms were prolonged in latency. Plasmapheresis were provided; clinical features improved. However, the electrophy-siological abnormalites remained. Thus we wish to report an additional case of woman suffering from the acute sensory neuronopathy, complementing the cases described by Stemm, Schaumburg and Asbury.


Assuntos
Feminino , Humanos , Potenciais de Ação , Braço , Ataxia , Proteínas do Sistema Complemento , Nervos Cranianos , Potenciais Somatossensoriais Evocados , Cinestesia , Perna (Membro) , Condução Nervosa , Plasmaferese , Reflexo de Estiramento , Couro Cabeludo , Sensação
3.
Journal of the Korean Neurological Association ; : 139-144, 1994.
Artigo em Coreano | WPRIM | ID: wpr-113858

RESUMO

A 67-year-old woman with brainstem abscess was cured by nonsurgical treatment. The clinical features and MRI findings allowed the presumptive diagnosis to be made. The abscess was located in the left midbrain part of brainstem; left ptosis and partial ophthalmoplegia with ellipticaI pupil. Massive antibiotic therapy was provided and clinical improvement was resulted. The authors reviewed reported cases and discussion was presented.


Assuntos
Idoso , Feminino , Humanos , Abscesso , Tronco Encefálico , Diagnóstico , Imageamento por Ressonância Magnética , Mesencéfalo , Oftalmoplegia , Pupila
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