Endogenous mast cell degranulation modulates cervical contractility in the guinea pig.
OBJECTIVE
The purpose of this study was to investigate the effect of endogenous mast cell degranulation on the contractility of isolated cervical strips from nonpregnant and pregnant guinea pigs.


METHODS
Longitudinal cervical strips from nonpregnant and pregnant (mid and term) guinea pigs were used for isometric tension recording. Responses to the mast cell degranulating agent, compound 48/80, were compared in the absence or presence of different inhibitors and receptor antagonists. Concentration-response curves were obtained to histamine and 5-hydroxytryptamine in strips that were incubated with antagonists or solvent.


RESULTS
Compound 48/80 and histamine significantly increased contractility of cervical strips in all 3 groups of animals. The inhibitor of mast cell degranulation significantly reduced responses to compound 48/80 and histamine-1 receptor antagonist reduced responses to histamine in all 3 groups. Histamine-1 receptor antagonist significantly inhibited responses to compound 48/80 in nonpregnant and mid pregnant guinea pigs. Histamine-2 receptor antagonist did not alter responses to compound 48/80 nor to histamine. The receptor antagonist 5-hydroxytryptamine-2 significantly inhibited cervical contractility that was induced by compound 48/80 in tissues from mid pregnant and term pregnant guinea pigs. Lipoxygenase inhibitor was effective in mid pregnant guinea pigs. Cyclooxygenase inhibitor, 5-hydroxytryptamine, and a combination of lipoxygenase and cyclooxygenase inhibitors had no effect on cervical contractility.


CONCLUSIONS
The degranulation of mast cells releases histamine and other mediators that stimulate cervical contractility through histamine-1 receptors. Cervical infiltration and modulation of contractility by mast cells may play an important physiologic and/or pathologic role in the control of cervical function during pregnancy.
Bytautiene
Egle
E
Department of Obstetrics & Gynecology, Division of Reproductive Sciences, The University of Texas Medical Branch, Galveston 77555-1062, USA.
Vedernikov
Yuri P
YP
Saade
George R
GR
Romero
Roberto
R
Garfield
Robert E
RE
D000818:Animals; D015550:Cell Degranulation / Q000502:physiology*; D002584:Cervix Uteri / Q000187:drug effects / Q000502:physiology*; D002744:Chlorpheniramine / Q000494:pharmacology; D002927:Cimetidine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D006168:Guinea Pigs; D006632:Histamine / Q000494:pharmacology; D006634:Histamine H1 Antagonists / Q000494:pharmacology; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008407:Mast Cells / Q000502:physiology*; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology*; D009994:Osmolar Concentration; D011247:Pregnancy; D011262:Pregnancy Trimester, Second; D011263:Pregnancy Trimester, Third; D012701:Serotonin / Q000494:pharmacology; D003189:p-Methoxy-N-methylphenethylamine / Q000494:pharmacology
D006634:Histamine H1 Antagonists; D006635:Histamine H2 Antagonists; D012701:Serotonin; D002744:Chlorpheniramine; D003189:p-Methoxy-N-methylphenethylamine; D002927:Cimetidine; D006632:Histamine