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Low Oxygen Drives Powerful Contractions During Labor

With each contraction during labor, the vessels supplying the uterine muscle compress, depriving the hard-working organ of oxygen. This transient hypoxia does not seem to hinder labor; instead, according to a new study in rat and human tissue [1], it has the effect of strengthening contractions. Researchers know very little about the mechanisms of labor. Pulses of oxytocin are known to drive contractions, but mice lacking oxytocin deliver their pups normally—suggesting that other factors contribute. It is also unclear how contractions become more powerful as labor proceeds. Mohammed Alotaibi et al. speculated that transient hypoxia during contractions might help propel labor. After all, they reasoned, some organs such as the heart and brain develop an adaptive, sometimes life-saving response to hypoxia, called hypoxic (or ischemic) preconditioning. This response involves cellular changes that shield the organ from damage. Could something similar be occurring during labor? To test this idea, the researchers exposed strips of uterine tissue—obtained from rats or from women undergoing cesarean sections—to various conditions and compounds. These strips pulsed with steady, regular contractions. When the researchers bubbled nitrogen instead of oxygen through the medium, in five minute episodes of hypoxia, the contractions transiently stopped during each episode—but subsequently gained strength (Fig. 1). These effects were observed only in tissue taken from females at term—but not earlier in pregnancy, for instance, women undergoing elective caesarean section at 38 to 39 weeks. In human tissue, the force of contractions increased by 112 percent, and in rats the effect was sustained for hours. The effects of hypoxia on contractions seem to be mediated by some of the same mechanisms that are thought to mediate hypoxic preconditioning, as suggested experiments on the rat tissue. These mechanisms include increases in acidity, adenosine, and ATP in the cellular milieu—as well as an increase in intracellular prostaglandins, which are also major stimulators of uterine activity. Oxytocin was not required for an increase in contractility in response to hypoxia, but oxytocin did bump up the force of these contractions. The researchers speculate that early activation of this mechanism for strengthening contractions might underlie some preterm deliveries, and that failures in the mechanism might contribute to poorly progressing labor. The findings also sound a note of caution for the early induction of labor—perhaps the uterine tissue may not be fully prepared to contract at full force, in response to hypoxia, until pregnancy runs its course and labor initiates naturally.