C.B. Martin

The urethral pressure profile in pregnancy and after delivery in healthy nulliparous women

Simultaneous urethrocystometry by means of a dual microtransducer catheter was performed according to a precise, standardized technique serially at 8, 16, 28, and 36 weeks of pregnancy and at 8 weeks post partum in 43 healthy nulliparous women. The urethral pressure profile at rest and the effect of stress (cough) on the urethral pressure profile during pregnancy and after delivery were measured. At each recording session, blood was obtained for determination of 17 beta-estradiol (E2), progesterone (P), and 17-alpha-hydroxyprogesterone (17-OH-PO). The continence parameters functional urethral length and urethral closure pressure, as well as the urethral closure pressure response to stress, did not change systematically during the course of pregnancy. Engagement of the presenting part at 36 weeks did not influence the urethral pressure profile measurements. Alterations in hormone levels during pregnancy were not correlated with the changes in urethral pressure profile measurements. Both urethral pressure and length parameters in all women who underwent vaginal delivery were notably decreased 8 weeks post partum when compared with early pregnancy values and with values obtained in a group of healthy nulliparous women in the follicular phase of the cycle. The decrease in length parameters was not observed in the six women in whom delivery was by cesarean section. The postpartum changes were not significantly correlated with the duration of the second stage of labor or with the presence or absence of an episiotomy. Also, no relationship with infant birth weight was found. Values of the urethral pressure profile parameters below the median value and defective transmission of pressure over the urethra were observed in almost all women who experienced stress incontinence during pregnancy and/or after delivery. These observations suggest that an inherent weakness of the urethral sphincter mechanism plays a key role in the pathogenesis of stress incontinence.

The clinical and urodynamic effects of anterior vaginal repair and Burch colposuspension

The clinical and urodynamic effects of anterior vaginal repair and Burch colposuspension for correction of stress urinary incontinence were assessed in a prospective study. Ninety women undergoing surgery for the first time because of genuine stress incontinence were studied. A full clinical examination including simultaneous urethrocystometry according to a standardized methodology with the patients in the supine, sitting, and standing positions was performed preoperatively, 3 months postoperatively, and again 1 to 2 years later. Clinical follow-up continued for 5 to 7 years. Neither surgical anterior vaginal repair nor Burch colposuspension affected the resting variables of the urethral sphincter mechanism. After Burch colposuspension the transmitted intraabdominal pressure to the urethra significantly increased in all recording positions in all women who were successfully treated. After successful anterior colporrhaphy, the increase in pressure transmission from the abdomen to the urethra was less prominent and was only present in the sitting and standing positions. The postural changes in the urethral pressure profile characteristic of stress urinary incontinence were still present even after successful restoration of continence. The impact of successful surgery for stress incontinence is the enhancement of transmission of the intraabdominal pressure rise to the proximal urethra. This is achieved primarily by anatomic alterations rather than by altering urethral sphincter function. Burch colposuspension was more effective for the correction of genuine stress incontinence than was anterior vaginal repair.

Urodynamic studies in the normal menstrual cycle: The relationship between hormonal changes during the menstrual cycle and the urethral pressure profile☆

The influence of endogenous gonadal steroids on the urethral pressure profile (UPP) was studied in 27 healthy nulliparous women with the normal ovulatory cycles. The UPP and hormonal values were recorded in the follicular phase, at midcycle, and early and late in the luteal phase. Simultaneous urethrocystometry was performed by means of the microtransducer technique, according to a precise standardized methodology. The parameters of the UPP, as defined by the Standardization Committee of the International Continence Society, and the area under the urethral closure pressure curve (integrated pressure) were calculated. Reproducibility of the UPP measurements was evaluated. In addition to a basal body temperature (BBT) chart, serum levels of 17 beta-estradiol (E2), progesterone (P), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin were measured at each study session in order to confirm a normal ovulatory pattern for that cycle and for comparison with the urodynamic parameters. The mean values and standard deviation of the UPP parameters in healthy nulliparous women in the supine and sitting positions are presented. Values of the pressure measurements obtained during one menstrual cycle did not change systemically with the hormonal alterations. At midcycle and early in the luteal phase, however, and anatomic and functional lengths of the urethra were consistently increased over those found in the early follicular and late luteal phases. The data suggest a causal relationship between the changes in serum E2 concentrations and the changes in urethral length.

Behavioural states in the fetuses of nulliparous women

Behavioural state observations were carried out serially on the fetuses of 14 low risk nulliparae. They were observed serially at 2-weekly intervals between 32 weeks gestational age and delivery at term. Two real-time ultrasound B-scanners were used to visualize fetal body, eye and breathing movements. Fetal heart rate patterns were recorded simultaneously by means of a clinical fetal monitor. States appeared to be present transiently in three fetuses at 34 weeks. States were definitely present in five of 13 fetuses studied at 38 weeks and six of seven observed at 40 weeks. In comparison to the fetuses of low risk multiparae studied earlier, the fetuses in the present study showed a somewhat lower proportion of quiescence (coincidence 1F) and higher percentage of activity (coincidence 2F); however, most of these differences were not statistically significant. In the fetuses which showed states, the distribution and durations of the states at 38 and 40 weeks were not different from those found previously in the fetuses of multiparae. We conclude that the development of behavioural states is generally similar in the fetuses of low risk nulliparae and multiparae, but that states appear at a somewhat later gestational age in the fetuses of nulliparae.

Postural blood pressure differences in pregnancy: A prospective study of blood pressure differences between supine and left lateral position as measured by ultrasound

Differences in blood pressure between the supine and left lateral positions were studied in pregnant subjects under standardized conditions with an automated ultrasound device. Cross-sectional studies were performed in 125 nulliparous pregnant women after the twenty-eighth week of amenorrhea and in 42 nonpregnant controls. Arterial blood pressure in the left lateral position was lower than in the supine position. This difference was due largely to differences in hydrostatic pressure. Large errors in measurement and regression to the mean contributed to wide spread in measured values. Neither hypertension nor pregnancy alone gave an enhanced postural difference in blood pressure. Hypertension in pregnancy was associated with a significantly larger positional change in diastolic blood pressure (D) than in systolic blood pressure (S). This study pleads for a standardized procedure for the measurement of blood pressure in gravidas in the supine position, for the detection of peripheral vasoconstriction in the supine position, and to compare clinical blood pressure studies in different institutions.

Effect of isoproterenol on uterine blood flow and cardiac output distribution in pregnant guinea pigs

The effects of isoproterenol, 0.05 micrograms X min-1 X kg-1 infused intravenously for 2 hours, on cardiac output distribution and uteroplacental blood flow were studied in six chronically catheterized guinea pigs between 60 and 68 days of pregnancy. Isoproterenol caused marked cardiac stimulation: Cardiac output was increased by 41%, of which 70% was distributed to the carcass and gastrointestinal tract. Absolute placental blood flow remained essentially unchanged, but the placental fraction of cardiac output decreased from 16% to 11%. Myometrial blood flow increased by 72%. Uteroplacental vascular resistance did not change significantly. In the guinea pig in late pregnancy beta-adrenergic receptors are present in the myoendometrial vessels but could not be demonstrated in the maternal vessels supplying the placenta.

Effect of ritodrine on uteroplacental blood flow and cardiac output distribution in unanesthetized pregnant guinea pigs

The effects of ritodrine, 15 micrograms X min-1 X kg-1 infused intravenously for 2 hours, on cardiac output distribution and uteroplacental blood flow were investigated in 10 chronically catheterized guinea pigs between 57 and 63 days of pregnancy. Ritodrine produced an average 29% increase in cardiac output, three quarters of which was distributed to the carcass and myocardium. Absolute placental blood flow decreased by 10%, and the placental fraction of cardiac output decreased by one third. Uteroplacental vascular resistance increased by 41% during ritodrine infusion. The proportional changes in placental blood flow were positively correlated and those in placental vascular resistance negatively correlated with the change in cardiac output.

The effect of maternal hyperoxia on breathing movements, body movements and rest-activity cycles of low-risk human fetuses

The effects of maternal hyperoxia on fetal breathing and body movements, and on fetal activity state as reflected in the fetal heart rate pattern, were studied in 20 healthy gravida. Fetal breathing and trunk movements were observed by means of real-time ultrasound scanning, and the fetal heart rate was recorded continuously before, during and after 30 min of maternal oxygen inhalation by mask. Maternal transcutaneous oxygen tension (TcPO2) was measured in 9 subjects. The protocol was also carried out in ten of the gravidas with substitution of compressed air for oxygen. Maternal TcPO2 nearly doubled during oxygen breathing in the subjects in whom this was measured. There were no significant changes in the incidence of fetal breathing or trunk movements, or in the distribution of heart rate patterns, during maternal oxygen breathing. Also, no differences were observed in these variables between the oxygen and compressed-air experiments. We conclude that the normal level of fetal oxygenation does not limit fetal activity in uncomplicated pregnancies.

Effect of prolonged infusion of ritodrine on uteroplacental blood flow and cardiac output distribution in unanesthetized pregnant guinea pigs

The effects of ritodrine, 15 micrograms X min-1 X kg-1 administered intravenously, on the maternal circulation and uteroplacental blood flow were investigated in eight chronically catheterized pregnant guinea pigs near term. Cardiac output and its distribution were measured by means of the radionuclide-labelled microsphere technique before, and after 2 and 6 h of infusion of ritodrine. Ritodrine produced a sustained elevation of cardiac output to 135 and 137% of the control value after 2 and 6 h, respectively. The carcass and gastrointestinal tract together accounted for the greatest portion of the extra blood flow, 77 and 84% at the times of the two flow measurements during treatment. After 2 h of ritodrine, mean placental blood flow was reduced to 85% of the control level (n.s.), uteroplacental vascular resistance was 127% of its initial value (n.s.), and the placental fraction of cardiac output had decreased from 18 to 12% (P less than 0.02). Continuation of the infusion to 6 h resulted in an increase in mean placental blood flow to 107% of the control value and return of uteroplacental vascular resistance to its initial level. The placental fraction of cardiac output increased to 14%, significantly (P less than 0.05) different from both the initial and the 2-h values. Blood flow to the skin, lungs, spleen and mammary glands decreased between the 2- and 6-h flow measurements. These observations are compatible with the hypothesis that the changes in uteroplacental blood flow during administration of ritodrine are passive, resulting from the balance between the increase in cardiac output and vasodilatation in extrauterine vascular beds.

The effect of a low-dose infusion of ritodrine on cardiac output distribution and uteroplacental blood flow in unanaesthetized pregnant guinea pigs

Cardiac output and its distribution were measured using the microsphere technique before and at 2 and 6 h during the infusion of ritodrine, 1.5 microgram X min-1 X kg-1 i.v., into near-term pregnant guinea pigs. Average cardiac output increased 16 and 25%, and total peripheral resistance decreased 16 and 19% after 2 and 6 h of ritodrine infusion. The carcass and gastrointestinal tract together received two-thirds of the extra cardiac output. Uteroplacental blood flow and uteroplacental vascular resistance were not significantly different from the preinfusion values after 2 h of ritodrine treatment, but were increased 35% and decreased 31%, respectively (p less than 0.05 and less than 0.01), after 6 h of infusion. The increase in uteroplacental blood flow between the 2- and 6-h measurements was positively, and the decrease in uteroplacental vascular resistance negatively correlated with the increase in cardiac output during the same period.