Infection and phagocytosis as possible mechanisms of rupture in premature rupture of the membranes.

The concept that premature rupture of the membranes is due to an infectious process is well accepted. However, no definitive data implicating a particular microorganism or a mechanism of action have been advanced. By the use of our recently developed experimental in vitro amnion-chorion reaction vessel model we have studied the effect of the peroxidase-hydrogen peroxide-halide antimicrobial system on these membranes. We have noted that amnion, chorion, decidua, and placental macrophages all possess peroxidase activity. Tissues collected from deliveries following labor (vaginal) are significantly higher in activity than those collected from deliveries with no labor (cesarean section). A mobilization of enzyme from macrophages to amnion appears to occur in the laboring patient. Increased protein hydrolysis is noted in membranes collected from patients without labor subjected to the peroxidase-hydrogen peroxide-halide cytotoxic system when compared with membranes from laboring patients. Bursting pressures of membranes collected from patients without labor are shown to be decreased when the membranes were incubated in the presence of lysolecithin or in the presence of amniotic fluid and phospholipase A2.