Modulation of rat uterine contractility by mast cells and their mediators

This study was designed to test the possibility that mast cells play a role in the regulation of uterine contractility.

Histamine and rat mast cell protease II levels were determined by radioenzymatic assay and standard radial immunodiffusion techniques, respectively, in uterine tissues from Wistar rats with timed pregnancies. Isolated uterine strips from nonsensitized and ovalbumin-sensitized nonpregnant and pregnant Wistar rats were used for isometric tension recording. Contractile responses to compound 48/80, carbachol, ovalbumin, normal rabbit serum, antirat immunoglobulin E, and 5-hydroxytryptamine were obtained. Antagonists methysergide, ketanserin, 5,8,11, 14-eicosatetraynoic acid, diphenhydramine, and sodium meclofenamate were also used.

Tissue levels of rat mast cell protease II and histamine were decreased during delivery compared with prepartum and postpartum levels. Carbachol and compound 48/80 stimulated uterine contractility, and responses were highest during late gestation (day 16 to term). Responses to ovalbumin of uterine tissues in rats sensitized to the antigen were highest at midpregnancy and decreased during the last 10 days of gestation. Ovalbumin challenge in vitro increased the frequency and magnitude of contractions in tissues from ovalbumin-sensitized rats. Compound 48/80 and antirat immunoglobulin E stimulated contractility in both control and sensitized rats. None of the antagonists prevented the contractile responses.

Activation of mast cells is an effective mechanism for stimulation of uterine contractility and may play an important role in the control of term and preterm parturition.