Jw. Walsh et al., PROGESTERONE AND ESTROGEN ARE POTENTIAL MEDIATORS OF GASTRIC SLOW-WAVE DYSRHYTHMIAS IN NAUSEA OF PREGNANCY, American journal of physiology: Gastrointestinal and liver physiology, 33(3), 1996, pp. 506-514
Women in pregnancy experience nausea, which correlates with gastric sl
ow-wave rhythm disruption. Mediators of these dysrhythmias were explor
ed. To quantitate slow-wave disruption, eight pregnant women with firs
t-trimester nausea underwent electrogastrography after a 250-kcal meal
. Results were compared with nonpregnant women with nausea during a pr
ior pregnancy who received estradiol and/or progesterone to levels of
the first trimester of pregnancy. Five pregnant women exhibited dysrhy
thmias, with increases in combined recording time in tachygastria plus
bradygastria, as well as decreases in the percentage of electrogastro
graphy signal power in the normal 3 cycle/min range (cpm), compared wi
th nonpregnant women (P < 0.05). Estradiol did not evoke dysrhythmias
in nonpregnant women; however, progesterone induced increases in recor
ding time in bradygastria plus tachygastria and increases in bradygast
ric signal power with corresponding decreases in signal power in the 3
-cpm range (P < 0.05). With estradiol and progesterone coadministratio
n, an additive effect was observed at 3.3 +/- 0.8 h, with increased re
cording time in bradygastria alone and in bradygastria plus tachygastr
ia with corresponding increases in bradygastric signal power and decre
ases in power in the 3-cpm range (P < 0.05). In conclusion, women with
nausea of pregnancy exhibit slow-wave rhythm disruption. Similar dysr
hythmias are evoked in nonpregnant women by progesterone alone or in c
ombination with estradiol in doses that reproduce levels in pregnancy.
Thus gastric dysrhythmias in pregnancy may be due to a combination of
elevated progesterone and estrogen levels.