Effects of Patient-Controlled Epidural Analgesia on Uterine Electromyography During Spontaneous Onset of Labor in Term Nulliparous Women.

OBJECTIVE: To investigate the effect of patient-controlled epidural analgesia (PCEA) on uterine electromyography (EMG) activity in term pregnant women during labor. METHODS: Nulliparous pregnant women in spontaneous term labor (N = 30) were enrolled (PCEA group, n = 20 and control group, n = 10). Five time periods (30 minutes each) were defined for noninvasive abdominal recordings and analysis of uterine EMG activity, that is, period I: before PCEA treatment with 2-cm cervical dilation; periods II to IV: each period successively at 30, 60, and 120 minutes after PCEA; and period V: second stage of labor with cervix at 10 cm dilation. Control patients without PCEA were monitored during the same times. The number of bursts/30 min, power density spectrum peak frequency, mean amplitude, and duration of uterine EMG bursts were measured to assess uterine EMG activity. Maternal, fetal, and labor characteristics were also recorded. Data were analyzed by analysis of variance followed by other tests. RESULTS: Electromyography parameters are significantly lower (P < .001) after PCEA (periods II to IV) compared to controls but similar between groups by period V (P > .05). Also, patients with PCEA have a slower rate of cervical dilation (P < .003, period IV only) and longer labor in both stage 1 and stage 2 (P < .05). All patients have similar (P > .05) positive labor outcomes. CONCLUSIONS: Patient-controlled epidural analgesia initially suppresses uterine EMG and slows cervical dilation thereby prolonging labor. However, the EMG activity recovers with labor progress with no effects on delivery outcomes.

PP014. A pioneer explore of PTZ-induced eclampsia in preeclampsia rats.

INTRODUCTION: Eclampsia is the most serious state of hypertensive disorder in pregnancy, but the pathogenesis of eclampsia seizures is poorly understood. OBJECTIVES: An eclampsia animal model was developed by PTZ injection on preeclampsia rats. METHOD: Rats received endotoxin (1.0µg/kg body weight) form tail vein in an hour on GD14 to build the preeclampsia (PE) model. PTZ i.p injection were given to PE rats on GD16, 17, 18 to induce seizures and build an eclampsia model. All experiment rats were divided into three groups, PE, normal, pregnant (P), non-pregnant (NP) group (n=18 in each group). Each group gave two doses of PTZ (40 or 35mg/kg) as subgroups. Blood pressure, urinary albumin, biochemical indexes (AST, ALT, SCr, Urea) were measured. Seizure severity was defined by Racine' standard and seizure time were recorded. RESULTS: PTZ-induced eclampsia shows a increasing blood pressure, urinary albumin, liver function damage and different stages of seizures. The latency of seizure in PE rats with 40mg/kg PTZ is obviously shortened when compared with the P and NP group (p<0.05) and the duration is prolonged (p<0.05). The same trend is still existence at the low dose of PTZ injection. Rate of tonic-clonic seizures is elevated in PE and P group when compared with NP group, but nonsignificantly. CONCLUSION: We use 40mg/kg PTZ to endotoxin induced preeclampsia model to build an eclampsia model, which mimicked the multiple organ function disorder in human eclampsia. Meanwhile, we found the PE status may decreases threshold for PTZ induced-seizures.