[Investigation of TNF-alpha converting enzyme and activity of nf-kb in tolerance to ischemia induced by intermittent normobaric hyperoxia in rat model]

Recent studies suggest that intermittent and prolonged normobaric hyperoxia [HO] results in ischemic tolerance to reduce brain injury. In this research attempts were made to see the changes in TNF-alpha converting enzyme [TACE] and NF-kB activity following intermittent HO and ischemia preconditioning. The rats were divided into two experimental groups, each consisted of 20 animals. The first group was exposed to 95% inspired HO for 4h/day for 6 consecutive days [intermittent HO; InHO]. The second group acting as the control was exposed to 21% oxygen in the same chamber [normobaric normoxia or room air; RA] continuously for six days [intermittent RA; InRA]. Each main group was subdivided to MCAO-operated [middle cerebral artery occlusion], sham-operated [without MCAO], and intact [without any surgery] subgroups. After 24hr, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score [NDS] and infarct volume were assessed in MCAO-operated subgroups. Immediately and 48 h after pretreatment, blood sampling for assessment of serum TNF-alpha levels were subjected. Then, the effect of intermittent HO and ischemia on NF-kB activity and TACE expression were measured. Preconditioning with intermittent HO and ischemia decreased NDS and infarct volume. Moreover InHO and MCAO-InHO upregulate TACE and increase NF-kB activity significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, InHO and ischemia seem to partly exert their effects via increase upregulation of TACE and NF-kB activity

Sofrimento fetal: fisiopatologia da lesao cerebral e prevencao por medicamentos / Fetal distress: pathophysiology of brain damage and pharmacologic interventions

O sofrimento fetal tem como consequencia final a lesao cerebral do feto. Este dano neurologico pode ser decorrente do insulto em si (periodo primario) ou se instalar na fase de reoxigenacao-reperfusao. Os seguintes fatores, isoladamente ou em associacao, participam da fisiopatologia da lesao cerebral no periodo perinatal: acidose intracelular, insuficiencia de trifosfato de adenosina, intoxicacao pelo calcio, aminoacidos excitatorios, radicais livres de oxigenio, expressao genica alterada e apoptose. O maior conhecimento desses mecanismos tem despertado muito interesse sobre o potencial de intervencao farmacologica na prevencao ou restricao da lesao cerebral no feto. Com essa finalidade, foram estudados os seguintes grupos de drogas: bloqueadores dos canais de calcio, antagonistas dos aminoacidos excitatorios, inibidores da cascata do acido aracdonico, antagonistas dos radicais livres de oxigenio e monosialogangliosideos...

Daño neurológico por preeclampsia-eclampsia: fisiopatología, prevención y tratamiento / Neurologic damage due to preeclampsia-eclampsia: physiolopathology, prevention and treatment

La preeclampsia-eclampsia se complica a menudo con alteraciones cerebrovasculares. Las manifestaciones clínicas son variables y el vasoespasmo es un problema habitual. Se presenta edema, trombosis, hemorragias, cambios fibrinoides transmurales, se pierde la autorregulación cerebral en las regiones dañadas y los trastornos iónicos transmembrana pueden ser la causa de convulsiones. El tratamiento preventivo de la preeclamsia-eclampsia consiste en el control de la presión arterial y del volumen intravascular, protección de las lesiones edoteliales e interrupción del embarazo. Las medidas específicas incluyen el empleo de glucocorticoides, clacioantagonistas, fenobarbital, flunitrazepan, clonazepan, difenilhidantoína y sulfato de magnesio intravenoso. El seguimiento de la enfermedad se hace mediante la evaluación frecuente del estado físico de la enferma, EEG, tomografía computada y resonancia magnética. Las emergencias quirúrgicas requieren de la presencia de un neurocirujano. En este artículo revisamos la fisiopatología, prevención y tratamiento del daño neurológico debido a la preeclampsia-eclampsia