Introduction

The prevention of preterm labour remains one of the primary goals of obstetric research. To achieve this effectively, we need to understand the mechanisms regulating uterine contractility, cervical ripening and activation of the fetal membranes. Whether preterm labour represents an acceleration of the mechanisms involved in term labour remains controversial. Romero et al. (1997) propose that the fundamental difference between term and preterm labour is that the former results from physiological activation of the components of a common terminal pathway, while preterm labour results from disease processes activating one or more of the components of this pathway. In contrast, Challis et al. (2000) suggest that the causes of preterm labour may vary at different times during pregnancy and will not necessarily reflect acceleration of the processes occurring during labour at term. At present, the factors maintaining myometrial quiescence during pregnancy, and those that stimulate the onset of uterine contractions and cervical ripening at term remain obscure. Until these factors are elucidated, it seems unlikely that effective strategies for the treatment of preterm labour will be found (Goldenberg and Rouse 1998).

Myometrial contractions

The uterus is spontaneously active and, using electromyographic measurements, contractile activity can be detected in both pregnant and non-pregnant women (Morrison 1996). Two different types of electromyographic activity have been described in the myometrium of the pregnant rhesus monkey, referred to as contractures and contractions, and are believed to be present in most species (Nathanielsz et al. 1992).