Effects of hypoxia on force produced by agonists and depolarization and arising spontaneously in the rat uterus.

The effects of cyanide and nitrogen on contractile activity in rat uteri was investigated. Hypoxia significantly reduced contractile activity produced either spontaneously, or by application of carbachol (50 mumol l-1) or oxytocin (20 nmol l-1) in preparations from pregnant and nonpregnant rats. Hypoxia had, however, significantly smaller effects on agonist-evoked than on spontaneous contractions. Application of agonists under hypoxic conditions restored some degree of force to preparations in which spontaneous activity had been abolished. This result suggests that the loss of spontaneous contractions was, in part, due to decreased excitability of the uterus, rather than to an impairment of the contractile machinery. Hypoxia significantly decreased the force produced by depolarization of the uterus. The effects of hypoxia on contraction produced by agonists or depolarization were not significantly different, suggesting that a similar mechanism may maintain force under these conditions, and that this mechanism does not occur during spontaneous activity. Lowering the external Ca2+ concentration to 0.1 mmol l-1 resulted in production of significantly less force in the presence or absence of agonist. The ability of hypoxia to decrease agonist-induced force was found not to be due to the intracellular acidification it produces. It was concluded that uterine hypoxia may decrease uterine contractions in vivo and a possible role in dystocia during labour was discussed.