A Very Brief History

Abstract

It stands to reason that a fetus, as it nears completion, needs a passage to the outer world that is commensurate with its size exactly at the time of parturition. The discrepancy between the pelvic canal and the fetus in most mammals is so large and the pelvis so rigid that a special mechanism must exist which corrects this discrepancy if a species is to persist. Here is one of the few examples where biology has to submit to reason. The birth canal cannot be opened during gestation because of the danger of premature fetal loss, and at the end of gestation the opening of the canal must be coordinated with a dramatic over-all shift of the endocrine balance which causes potentially damaging uterine contractions. This set of circumstances is well known to endocrinologists and explains Hisaw’s experiments with pregnant guinea pig serum. Only a hormone could cause such a change, and most hormones travel from the gland of origin to the site of action by the blood stream. Serum from pregnant animals with relaxed symphyseal joints was a plausible place to search for this factor. Once virgin guinea pigs had been treated with estrogen they responded to the pregnancy serum by significant widening of the symphysis pubis.1 This was a momentous discovery albeit overshadowed by the discovery of insulin, the pancreatic disulfide homologue of relaxin, at about the same time. Insulin took center stage at once because it saved lives and relaxin fell by the wayside because humans had developed a surgical procedure to overcome the problems of pelvic insufficiency. Nonetheless, relaxin researchers had an inkling that insulin and relaxin had something in common (Fig. 2.1). A condensed pictorial summary of both factors as they evolved through their stages of discovery is shown in Figure 2.2.