Modeling the propagation of uterine electrical activity

Changes in the physiological uterine activity have been associated with the progression of pregnancy and the onset of labor: during pregnancy, the uterus is usually relatively quiescent while the cervix is rigid and closed, whereas during labor, the uterus exhibits rhythmic and coordinated forceful contractions while the cervix softens and dilates for successful expulsion of the fetus. These uterine contractions appear because of propagated electrical activity generated at cellular levels in its myometrial cells and propagate through gap junctions [1-2]. The uterine electrical activity has been extensively studied. The recorded signal, called the uterine electromyogram (EMG), has been proposed as a new technique to evaluate contractile activity of the uterus. Therefore, uterine EMG was widely investigated in order to predict the risk of preterm labor and subsequent preterm birth. In this context, many studies were devoted to the study of the propagation of the uterine electrical activity as a new complementary tool for improving preterm labor diagnosis. Modeling the electrical activity generated at cellular level is thus an important tool for understanding the propagation mechanisms and their relationship with the uterine EMG signal recorded externally from the abdominal wall of the pregnant women. The first model was developed from the ionic channels found in the uterine cells. The first step was to simulate the electrical activity at a cellular level. In [3], Rihana et al. described the development of a mathematical model based on experiments voltage clamp based on the results of previous work [4-5]. This model was based on the formulation of Hodgkin and Huxley, and was adapted to the specificity of a uterine cell. The first results of this model permitted to validate the physiological effects of certain pharmacological agents known for their effects on the uterine excitability. Through the dynamical analysis of the model, we have demonstrated how some substances such as calcium channel blockers or potassium channel openers inhibit the excitability the uterus. This explains the tocolytic effect that extends the period of pregnancy and prevents the preterm labor. The second step consisted of the integration of the cellular model in the propagation model in two-dimension (reaction-diffusion equations) in order to propagate the electrical activity to a tissue level. We have simulated the increase of the conductivity due to the increase of the number of the gap junctions which leads to a new synchronous propagation of the uterine activity as well as to an increase of the conduction velocity. The simulated results were compared with previous experimental results reported in the literature [6]. A simplified version of the spatiotemporal integration phenomenon of the electrical activity resulted to the reconstruction of a first example of surface EMG. The preliminary work on modeling the uterine electrical activity is interesting and must be followed by a further work. First, it would be interesting to study the propagation at a tissue level in order to define the position, the percentage and number of pacemaker areas in the uterine tissue, the distribution of gap junctions, and orientation of uterine fibers. Moreover, in order to reach the abdominal level, it is important to develop new approaches to move from the tissue level (current model) to the organ level (abdominal uterine EMG) without facing time and capacity computer calculation problems. The simulation of the signal at the abdominal level will allow connecting the different phenomena that are related to the generation and the propagation of the uterine electrical activity, whether in normal or pathological state, to the surface EMG signal, the only signal that can be used for clinical applications.