RESUMO
The angiotensin II receptor subtype 2 (AT2-R) has been proposed to mediate protective vascular actions after brain injury. In this study we investigated the participation of this peptide in the tolerance to cellular damage induced by preconditioning in a rat model of neonatal hypoxia-ischemia (HI). We found that injured animals present a decreased number of microvessels in the ipsilateral (IPLT) side of the brain while in the contralateral (CNLT) side the microvessel number is increased. On the contrary, in the preconditioned animals the microvessels maintained the same number as in control animals. However these vessels show a remarkable increase of the fluorescent signal when they are labeled with antiFlk-1 (VEGFR2), while the Flt-1 (VEGFR1) signal faded in both the injured and the preconditioned animals. The pharmacological blockade of the AT2-R by the drug PD123319 (1.69 mM in the lateral ventricle) diminished the resilience of the microvasculature to HI injury provided by preconditioning and also the Flk-1 increase that occurred in these animals. In conclusion these results suggest an interaction of the AT2-R with VEGFR2 in the neonatal brain microvasculature that produces protective effects which are associated with injury tolerance.
Assuntos
Hipóxia-Isquemia Encefálica/metabolismo , Microvasos/fisiopatologia , Receptor Tipo 2 de Angiotensina/metabolismo , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo , Bloqueadores do Receptor Tipo 2 de Angiotensina II/farmacologia , Animais , Animais Recém-Nascidos , Encéfalo/irrigação sanguínea , Encéfalo/efeitos dos fármacos , Encéfalo/crescimento & desenvolvimento , Encéfalo/patologia , Hipóxia Fetal/metabolismo , Hipóxia Fetal/fisiopatologia , Hipóxia-Isquemia Encefálica/fisiopatologia , Hipóxia-Isquemia Encefálica/prevenção & controle , Imidazóis/farmacologia , Precondicionamento Isquêmico , Microvasos/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Piridinas/farmacologia , Ratos , Ratos Wistar , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/metabolismoRESUMO
Complications act as stress-inducers during pregnancy so the fetus can develop functional compensatory mechanisms or morphologic changes. The cases analyzed are with congenital malformations or acute stress; chronic included cases with ascending infection (AI) and perinatal hypoxia/anoxia (PHA). The hematoxylin-eosin (H&E) was done to analyze the vacuolization, and the immunohistochemistry to the phagocytosis. The discreet standard of vacuolization was observed in 52.6% of the cases, 22.1% moderate, and 25.3% severe. The number of macrophages was higher in PHA. Changes in these organs are closely related to the cause of death and to the period during which the harmful agent.
Assuntos
Infecções Bacterianas/patologia , Morte Fetal , Doenças Fetais/patologia , Mortalidade Infantil , Complicações Infecciosas na Gravidez/patologia , Estresse Fisiológico , Córtex Suprarrenal/embriologia , Córtex Suprarrenal/metabolismo , Córtex Suprarrenal/patologia , Adulto , Infecções Bacterianas/metabolismo , Infecções Bacterianas/mortalidade , Contagem de Células , Anormalidades Congênitas , Feminino , Doenças Fetais/mortalidade , Hipóxia Fetal/metabolismo , Hipóxia Fetal/mortalidade , Hipóxia Fetal/patologia , Idade Gestacional , Humanos , Recém-Nascido , Infecções , Macrófagos/patologia , Gravidez , Complicações Infecciosas na Gravidez/metabolismo , Complicações Infecciosas na Gravidez/mortalidade , Nascimento Prematuro , Timo/patologia , Vacúolos/patologiaRESUMO
Because chronic hypoxemia causes a redistribution of iron from serum and storage pools into an expanding erythrocyte mass, and because infants of diabetic mothers are often hypoxemic in utero and have a high prevalence of polycythemia at birth, we studied iron distribution in 43 term infants of diabetic mothers. Twenty-four infants were at an appropriate size for gestational age; 19 were large for gestational age. At birth, 28 infants (65%) had abnormal serum iron profiles; eight had decreased ferritin concentrations only (stage 1), nine had decreased ferritin and increased total iron-binding capacity values (stage 2), and 11 had these serum findings plus elevated free erythrocyte protoporphyrin concentrations (stage 3). The hypoglycemic infants who were large for gestational age (n = 14) had a higher prevalence of abnormal iron profiles than euglycemic infants who were appropriate in size for gestational age (n = 20; 93% vs 50%; p = 0.009). Progressively abnormal iron profiles were associated with higher glycosylated fetal hemoglobin values, greater degrees of macrosomia, increased hemoglobin and erythropoietin concentrations, and increased erythrocyte/storage iron ratios. Erythropoietin concentrations were inversely linearly correlated with serum iron values (n = 32, r = -0.54; p = 0.003). The combined erythrocyte and storage iron pools were significantly lower in infants with abnormal iron values whose mothers were diabetic, particularly in infants of women with confirmed diabetic vasculopathy. We speculate that these findings are likely due to (1) increased fetal iron utilization during compensatory hemoglobin synthesis in response to chronic hypoxemia and (2) reduced iron transfer during late gestation complicated by diabetes.
Assuntos
Complicações do Diabetes , Hipóxia Fetal/etiologia , Ferro/metabolismo , Gravidez em Diabéticas , Peso ao Nascer , Feminino , Ferritinas/análise , Hipóxia Fetal/sangue , Hipóxia Fetal/metabolismo , Humanos , Recém-Nascido , Ferro/sangue , GravidezRESUMO
Acute fetal asphyxia resulting from maternal blood loss and hypotension causes a reduction in the incorporation of precursors into disaturated phosphatidylcholine, the principal lipid in the pulmonary surfactant. Treatment of the maternal hypotension is associated with return of fetal lung DSPC synthesis to control levels by 72 hours.