Preterm birth, frequently associated with maternal genital tract infection, is the leading cause of perinatal mortality and morbidity. A greater understanding of the pathophysiology of chorioamnionitis and preterm labor is necessary to devise appropriate strategies for diagnosis and treatment. Human studies have been cross-sectional in design and have not established causal relationships between specific bacteria, chorioamnionitis, mediators of inflammation and preterm labor. The objective of this research plan is to develop an animal model in pregnant rhesus monkeys to study the pathophysiologic mechanisms in the development of premature labor associated with infection of the decidua and chorioamnion. We plan to inoculate known concentrations of specific microorganisms including both a gram positive microorganism, Group B Streptococci and a gram negative, endotoxin-producing organism, Escherichia coli, into the amniotic fluid or choriodecidual space and to conduct physiological and biochemical studies in unanesthetized chronically catheterized maternal-fetal preparations in a mobile tether assembly. We will attempt to answer the following questions: 1) Does infection of the decidua, chorioamnion or amniotic fluid by specific microorganisms result in the premature onset of labor? 2) What is the sequence of physiological and biochemical events in the evolution of preterm labor associated with intrauterine infection? 3) Are the qualitative or quantitative patterns in uterine activity associated with infection different compared to spontaneous labor at term?
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