RESUMO
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.
Assuntos
Hipóxia Fetal/metabolismo , Fosfatidilcolinas/biossíntese , Acidose Respiratória/complicações , Animais , Radioisótopos de Carbono , Feminino , Hipóxia Fetal/complicações , Humanos , Recém-Nascido , Pulmão/irrigação sanguínea , Ácidos Palmíticos/metabolismo , Fosfatos/metabolismo , Radioisótopos de Fósforo/metabolismo , Gravidez , Síndrome do Desconforto Respiratório do Recém-Nascido/etiologia , OvinosRESUMO
Ovine placental lactogen, purified from term sheep cotyledons, has been found to have chemical and biologic properties similar to those of human placental lactogen, ovine growth hormone, and ovine prolactin. OPL stimulates lactation in vivo and in vitro and binds to prolactin and growth hormone membrane receptors. Its binding to growth hormone receptors is approximately 20 times greater than that of hPL, suggesting that its somatotrophic potency is greater than that of hPL. Preliminary in vivo studies in the sheep indicate that oPL affects maternal carbohydrate, lipid, and protein metabolism and that its effects are, in part, similar to those of hPL and growth hormone.