Concomitant Reduction in Uterine Blood Flow and Intrauterine Oxygen Tension in the Rat Following Nicotine Administration

Abstract

It is well established that cirgarette smoking adversely affects pregnancy (see: Weathersbee, 1980a). Many of the deleterious actions of tobacco use during pregnancy are thought to result from nicotine, the principal alkaloid of tobacco. Nicotine exerts diverse effects on the endocrine system, thereby influencing the initiation, course and outcome of pregnancy. In addition to modifying gonadotropin secretion (Blake et al., 1972; Yoshinaga et al., 1979), the alkaloid evokes the release of catecholamines (Resnik et al., 1979) which in turn constricts the uterine vasculature (Anderson et al., 1977) and alters the intrauterine environment (Hammer et al., 1981). Indeed, inhalation of cigrarette smoke produces transient fetal hypoxia (Manning and Feyerabend, 1976). While such events in late pregnancy may impair fetal well-being, pregnancy wastage occurs very frequently during the peri-implantation period (see: Weathersbee 1980b). Though unattached to the uterus, the conceptus nevertheless grows at a rapid rate and its metabolic needs proceed pari passu as the time for implantation approaches. Such increased metabolic demands, prior to the establishment of sufficient blastocystuterine contact, render the conceptus particularly vulnerable to suboptimal supplies of oxygen and other metabolic substrates. In the rat for example, administration of nicotine during early pregnancy suppresses conceptus growth (Hammier et al., 1981), impairs uterine decidualization (Card and Mitchell, 1978), and retards implantation (Card and Mitchell, 1979). Since the process of nidation is dependent on a number of vascular-related events, the following study was undertaken to determine the relationship between uterine blood flow and the availability of oxygen within the uterus and the effects of nicotine on such vascular-dependent phenomena as blood flow and capillary permeability at the implantation site.