ABSTRACT
BACKGROUND: Exposure of the spinal cord in myelomeningocele (MM) throughout gestation increases spinal injury. Astrocyte activation evidenced by glial fibrillary acidic proteins (GFAP) indicates the extent of injury. Corticosteroids modulate GFAP synthesis, but their effect in MM is unclear. The purpose of this study was to evaluate the GFAP expression in a fetal rat model of dysraphism and the effect of corticosteroid treatment on this marker and on clinical neurological disabilities. METHODS: Dysraphism was surgically created in 2 groups of 48 rat fetuses; group 1: control, and group 2: treated with corticosteroid. Each group was subdivided into fetuses with surgically created MM, controls and shams on day 18.5 of gestation (term = 22 days). Fetuses were harvested on day 21.5, examined for evidence of neurological deficits, and the following clinical parameters were registered: kyphosis, tail deformities, leg deformities, leg paralysis or paresis and pain perception. The fetuses were fixed for GFAP immunostaining. RESULTS: All fetuses with MM in group 1 presented neurological deficits and glial reactions with GFAP expression, as opposed to controls and shams. In group 2, corticosteroid treatment prevented some neurological deficits (18-25%), reducing glial response and GFAP expression. CONCLUSIONS: Experimentally induced dysraphism in the rat fetus is related to glial response and increased GFAP expression in the spinal cord. Corticoid treatment clinically improved nerve injury in some fetuses. It reduced glial reaction and GFAP expression.
Subject(s)
Adrenal Cortex Hormones/pharmacology , Glial Fibrillary Acidic Protein/metabolism , Spinal Cord Injuries/drug therapy , Spinal Cord Injuries/metabolism , Spinal Dysraphism/drug therapy , Spinal Dysraphism/metabolism , Animals , Biomarkers/metabolism , Disease Models, Animal , Female , Gliosis/drug therapy , Gliosis/metabolism , Gliosis/pathology , Male , Pregnancy , Rats , Rats, Sprague-Dawley , Spinal Cord/metabolism , Spinal Cord/pathology , Spinal Cord Injuries/pathology , Spinal Dysraphism/pathologyABSTRACT
UNLABELLED: Fetuses with digestive anomalies such as gastroschisis may present intrauterine growth restriction (IUGR) and shortened intestines. OBJECTIVE: The aim of this study was to assess the influence caused by amniotic fluid (AF) in intestinal length and somatic growth in an experimental gastroschisis fetal model at two distinct gestational ages. MATERIAL AND METHOD: Fetal rats were operated according to Correia-Pinto on 2 different days of gestation: day 18.5 (group I) and day 19.5 (group II). Each group was divided into three sub-groups: fetuses with gastroschisis (G), control (C) and sham(S). Body measurements and histological analysis were done. RESULT: Body measurement analysis showed: average body weight (g) in group I was G = 5.32, C = 5.68, S = 5.86; group II was G = 5.32, C = 5.80, S = 5.66. Average intestine weight (g) in group I was G = 0.283, C = 0.238, S = 0.231; group II was G = 0.272, C = 0.231, S = 0.233. Average intestine length (mm) in group I was G = 125, C = 216, S = 209; group II was G = 148, C = 226, S = 226. Histological analysis showed a decrease in the number and size of the intestinal microvillae and a light edema of serosa. CONCLUSION: Gastroschisis had a direct correlation with IUGR and the time of exposure of the fetuses to AF had no influence on body weight in gastroschisis fetuses but did interfere with intestinal length.
Subject(s)
Amniotic Fluid/physiology , Fetal Development/physiology , Fetal Growth Retardation/physiopathology , Gastroschisis/physiopathology , Intestines/growth & development , Animals , Body Size/physiology , Disease Models, Animal , Fetal Growth Retardation/etiology , Fetal Organ Maturity/physiology , Gastroschisis/complications , Gestational Age , Organ Size/physiology , RatsABSTRACT
UNLABELLED: Dysraphism is a defect in neural tube development, leading to dysplastic growth of the spinal cord and meninges. Myelomeningocele (MM) is just one of its forms. Hydrocephalus is among the most important alterations in MM and occurs as a consequence of Arnold-Chiari malformation (AC). Experimental models have been developed in sheep, rabbits and rats to study MM physiopathology, allowing a more detailed evaluation of clinical parameters involved in this anomaly. OBJECTIVE: Using the experimental model of dysraphism in fetal rats, the aim of this study was to evaluate the relevance of AC malformations, clinical parameters and grade of histological lesions. MATERIALS AND METHODS: Three groups with 16 fetuses in each were compared, MM, Control and Sham, after intrauterine surgical creation of MM on day 18.5 of gestation (term = 22 days). AC was evaluated by photographic comparison of sagittal cuts of fetal heads. Clinical and histological evaluations were also made. RESULTS: 88% of AC (14/16) in MM fetuses were obtained, besides 100% of clinical alterations. Necrosis and erosion of the spinal cord exposed to amniotic fluid were verified in histology. CONCLUSION: The presence of AC in the dysraphism rat model was high. These results allowed the use of this model to study alterations and intrauterine evolution of MM in a fashion similar to those observed in humans.
