PubMed · 11366390
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1999-03-05. Oral argument set.. https://pubmed.ncbi.nlm.nih.gov/11366390/
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A basic understanding of the mediators and related mechanisms involved in the genital physiology of the female sexual response, and, in particular, the physiology of arousal, is paramount for the clinical practitioner whose medical knowledge and practice pertain to female sexual dysfunction. Familiarity with established and evolving scientific principles relating to female genital physiology offers insight into functional aspects as well as disturbances of function relating to the female sexual response. Improved knowledge with regard to the central and peripheral nervous system components of female genital responses, chemical mediators, including endocrine factors determining the female sexual response, and other cellular and subcellular mechanisms should advance pharmacologic management for female sexual arousal disorder.
Changes induced by human sexual arousal serve reproductive and recreational functions. The current sexual phase model (desire, excitation, orgasm, and resolution) conveys little about this duarchy. Lack of spontaneous sexual desire in a third of nonclinic females indicates that the D phase needs splitting into D1 (the spontaneous [endogenous] activation of desire) and D2 (desire activated by sexual excitation at and during the E phase). Attempts to link D1 with reproduction by studies monitoring it over the menstrual cycle revealed a D1 peak just before or at ovulation, but its reliability is criticized because of the poor identification of the time of ovulation. Sexual arousal initiates enhanced genital blood flow, leading to the formation of a neurogenic transudate, lubricating the vagina, partly buffering its acidity, and increasing its oxygen tension all features that enhance spermatozoal function and survival. Orgasm occurs with vaginal and uterine contractions. The latter have been misinterpreted as powering rapid sperm transport to facilitate fertilization, but such fast transport would lead to the tubal deposition of noncapacitated, incompetent spermatozoa. Vagino-cervico elevation, however, delays rapid sperm transport and allows the initiation of decoagulation and sperm capacitation before the elevation resolves. The fastest transport of spermatozoa from cervix to the fallopian tubes occurs in the nonaroused female by uterine/subendometrial smooth muscle peristalsis. There is some evidence that even this may be reduced for a time after coitus, adding to the transport delay. If a number of the changes induced by sexual arousal are inadequately expressed, sexual as well as reproductive dysfunctions could arise.