Hiperoxia por dos horas produce daño morfológico cerebral luego de asfixia neonatal experimental / Two-hour hyperoxia following experimental neonatal asphyxia produces morphological brain damage

Objetivos: Determinar el efecto de una exposición de dos horas de hiperoxia al 21%, 40% y 100% sobre la morfología cerebral, en un modelo experimental de asfixia neonatal. Diseño: Estudio experimental. Institución: Instituto Nacional de Salud del Niño, Lima, Perú. Material biológico: Ratas albinas Holtzmann. Intervenciones: Ciento veinte ratas albinas Holtzmann de una semana de nacidas (a excepción del grupo control) fueron sometidas a asfixia experimental por ligadura de la arteria carótida izquierda y luego expuestas a hipoxia (oxígeno al 8%). Después fueron asignadas aleatoriamente a uno de los siguientes grupos: exposición por dos horas a O2 al 100%, a O2 al 40%, a O2 al 21% y un grupo control (no expuesto a asfixia experimental). El daño cerebral fue evaluado mediante la medición del peso cerebral y el porcentaje del área cerebral con daño microscópico. Principales medidas de resultados: Daño cerebral. Resultados: El peso cerebral promedio fue menor en los animales de los grupos sometidos a hiperoxia experimental (ANOVA; p<0,001). Se presentó daño cerebral microscópico con mayor frecuencia en el grupo sometido a hipoxia experimental que recibió O2 100% por dos horas y con menor frecuencia en el que recibió O2 al 40% (60% versus 43,3%), diferencia que fue estadísticamente significativa (prueba χ²; p<0,001). El grupo sometido a hipoxia experimental que recibió O2 100% tuvo un mayor porcentaje promedio de área cerebral con daño microscópico (18,3%), en comparación con los otros grupos de hipoxia experimental, aunque la diferencia no fue estadísticamente significativa (ANOVA; p=0,123). Conclusiones: La hiperoxia al 100% por dos horas se asoció con menor peso cerebral y mayor daño cerebral en animales de experimentación sometidos a asfixia neonatal experimental.

Objectives: To determine the effect of 2-hour exposure to 21% O2, 40% O2 and 100% O2 on cerebral morphology in an experimental model of neonatal asphyxia. Design: Experimental study. Setting: Instituto Nacional de Salud del Niño, Lima, Peru. Biologic material: Holtzman albino rats. Interventions: A sample of 120 one week-old Holtzman albino rats (with the exception of the control group) underwent experimental asphyxia by left carotid artery ligation and then exposition to hypoxia (8% O2); thereafter rats were randomly assigned to one of the following groups: exposition for two hours to 100% O2, to 40% O2, to 21% O2, and a control group (not exposed to experimental asphyxia). Brain damage was determined by brain weight and percentage of microscopic brain area damage. Main outcome measures: Brain damage. Results: Brain weight was lower in animals with experimental hyperoxia (ANOVA, p<0.001). Microscopic damage was more frequent in the group receiving 100% O2 for two hours and with less frequency in the group receiving 40% O2 (60% versus 43.3%). The difference was statistically significant (χ2 test: p<0.001). The group receiving 100% O2 had more microscopic brain damage (18.3 %) in comparison with the other groups of experimental hypoxia, but the difference was not statistically significant (ANOVA, p=0.123). Conclusions: Following neonatal asphyxia 100% two-hour hyperoxia was associated with less brain weight and more damage in experimental animals.

Hyperoxia with 100% oxygen following hypoxia-ischemia increases brain damage in newborn rats.

OBJECTIVE: To describe the effect of reoxygenation with 100% O2 as compared to the effect of room air in newborn rat brains after asphyxia. METHODS: Experimental asphyxia (carotid artery ligation followed by hypoxic exposure with 8% O2 for 2 h) was performed on 7-day-old rats. After hypoxia-ischemia the rats were reoxygenated with either 100% O2 (hyperoxia group) or 21% O2 (room air group) for 24 h and then returned to the dam. The rats were killed 1 week after the experiment to study the cerebral cortex and hippocampus. RESULTS: Rats reoxygenated with 100% O2 post-asphyxia showed more frequency of cortical damage (10 of 24 rats) than those reoxy genated with room air (3 of 24 rats) (chi2 test, p = 0.02). CONCLUSION: We consider that hyperoxia with 100% oxygen after hypoxia-ischemia can cause more damage in the cerebral cortex than room air in newborn rats.

Effect of propentofylline on hypoxic-ischaemic brain damage in newborn rat.

BACKGROUND: Studies showed that propentofylline enhances the action of adenosine and protects hippocampal neuronal damage against transient global cerebral ischaemia. Our study was to investigate the effect of propentofylline on hypoxic-ischaemic brain damage in neonatal rat. METHODS: Seven-day-old Wistar rats were subjected to unilateral common carotid artery ligation and hypoxia in oxygen 8 kPa for two hours at 37 degrees C. Propentofylline (10 mg/kg) was administered intraperitoneally one hour after hypoxia-ischaemia (treated group). Control group rats were received an equivalent volume of saline. The effects of propentofylline were assessed by observing the body mass gain, behavioural alteration and neurohistological changes. The rats were sacrificed at 72 hours after hypoxia-ischaemia, and the brain sections were examined after haematoxylin and eosin staining. RESULTS: The propentofylline-treated rats had better body mass gain and better behavioural response than the paired saline-controls did. In the control group, the rats either lost body mass or had little mass gain after the insult, their average body mass gain was 97.3% at 24 h, 100.3% at 48 h, and 114.1% at 72 h of recovery. In propentofylline-treated group, there was a significant improvement of body mass gain at 24 h (100.2%, P < 0.05) and 48 h (110.3%, P < 0.01) of recovery; the percentage of rats that performed well on behavioural test was significantly higher from 48 h to 72 h of recovery (P < 0.05); the incidence of severe brain damage to the cerebral cortex and dentate gyrus was significantly reduced in propentofylline-treated rats (cortex, 93% - 70.8%, P < 0.01; dentate gyrus 95% - 66.7%, P < 0.01) as compared with control rats. CONCLUSIONS: Administration of propentofylline 1 hour after hypoxia-ischaemia significantly attenuates brain damage in both the cerebral cortex and dentate gyrus, and also improves the body mass gain as well as behavioural disturbance in 7-day-old rats.

Usefulness of percutaneous intracardiac administration of colored microspheres in measuring blood flow distribution to the brain in 7-day-old rats.

OBJECTIVE: By using colored microsphere (CMS) technique in newborn rats, we explored the relationship between injection sites and blood flow distribution patterns in open-chest and in closed-chest models, with hopes that percutaneous left ventricle injection can be applicable to measure relative blood flow distribution to the brain. METHODS: Seven-day-old Wistar rats were used. In open-chest models (n = 30), we exposed the heart and injected CMS (15 microm diameter, 125000 spheres in 0.05 mL) to left and right ventricles, respectively. In closed-chest models (n = 12), we percutaneously punctured the left ventricle to administer microspheres to see the difference in blood flow distribution between the right and left side of organs. Microsphere counts were compared between the left and right side of each organ by unpaired t-test (mean +/- SD). RESULTS: Open-chest showed that right ventricle injection resulted in exclusive entrapment in the lungs, while left ventricle injection resulted in systemic distribution. According to this, one of 12 injections in the closed-chest was judged as right ventricle injection. The other 11 showed insignificant differences between the right and left side in the cortex, lung, and kidney. CONCLUSION: Right ventricle injection is differentiated from left ventricle injection and microsphere counts are the same between right and left side of the organs, suggesting that percutaneous microsphere injection is applicable for relative blood flow distribution in 7-day-old rat models.

Apéndice caudal con lipoma invasivo / Human tail with invasive lyphoma

Este reporte describe la presencia de un apéndice caudal o cola de 7cm de longitud en un recién nacido.