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A randomized controlled study was carried out at three medical centers to compare the efficacy and side effects of ethanol and ritodrine in the treatment of threatened premature labor. One hundred and thirty-five patients judged to be between the twentieth and thirty-sixth week of gestation and presenting with clinical symptoms of premature labor were included. Sixty-seven patients were treated with intravenous infusion of 10 per cent ethanol. Sixty-eight patients were treated with intravenous infusion of ritodrine for 12 hours followed by oral ritodrine. If labor recurred prematurely, up to two additional courses of ethanol or ritodrine were given. Delivery was postponed for more than 72 hours in 49 of 67 patients (73 per cent) with ethanol and in 61 of 68 patients (90 per cent) with ritodrine; this difference was significant. Patients in the ethanol group gained a mean of 27.6 days while patients in the ritodrine group gained a mean of 44.0 days. Fifty-four per cent of the ethanol group and 72 per cent of the ritodrine group carried their infants to 36 weeks of gestation. Five infants in the ethanol group and one infant in the ritodrine group died from respiratory distress syndrome. The most frequent side effect of ethanol were nausea and vomiting. The most frequent side effects of ritodrine were tachycardia and blood pressure changes which were easily controlled by lowering the infusion rate. Ethanol and ritodrine were both found to be effective inhibitors of premature labor with ritodrine giving the most favorable results.
Ritodrine hydrochloride was administered parenterally to pregnant ewes during spontaneous or oxytocin-induced uterine activity. The effects of ritodrine on the uterus and cardiovasculature were assessed both with and without simultaneous administration of either alpha or beta blockade. Ritodrine was found to be an effective inhibitor of both spontaneous and induced uterine activity. Ritodrine did cause maternal tachycardia but no significant hypotension. Alpha-adrenergic blockade did not influence the effects of ritodrine. Beta blockade with propranolol reversed the uterine and cardiovascular effects of ritodrine, whereas beta blockade with practolol reversed the cardiovascular effects without interfering with the inhibition of uterine activity produced by ritodrine.
The response of the fetal circulation to beta adrenergic stimulation with ritodrine hydrochloride has been investigated by long-term monitoring of the fetal lamb in utero. Ritodrine was infused intravenously either into the ewe or directly into the fetus, and cardiovascular and acid-base responses were measured. Fetal cardiac output and its distribution were measured with the use of radionuclide-labeled microspheres. The output of each ventricle also was measured by means of long-standing implanted electromagnetic flow transducers around the ascending aorta or pulmonary trunk during infusion of ritodrine at various rates into the fetus. Infusion of ritodrine (1.9 mcg. per kilogram per minute) into the ewe caused no change in fetal heart rate, blood pressure, cardiac output, or umbilical blood flow, but did cause an increase in fetal adrenal and myocardial blood flow. Ritodrine infused directly into the fetus produced a marked increase in fetal heart rate and a minimal change in cardiac output. There were no significant changes in fetal or maternal acid-base balance during the ritodrine infusions.
The effect of ritodrine upon uterine artery blood flow (UtBF) and umbilical vein blood flow (UmBF) was investigated in near-term chronic sheep preparations. During intravenous ritodrine infusions to the ewe in sequential dose rates from 100 to 800 mug per minute, UtBF fell progressively to 43 per cent below control levels and mean maternal arterial pressure (MMAP) declined 20 per cent. During constant infusions of 100, 400, or 800 mug per minute of ritodrine to the ewe for 120 minutes,, UtBF decreased 10, 37, and 31 per cent, respectively, and MMAP decreased 6, 20 and 25 per cent respectively. Dose-related maternal tachycardia and hyperglycemia occurred. There were no significant changes in UmBF, mean fetal arterial pressure, or fetal heart rate. During all infusions, maternal and fetal arterial pH, PCO2, and PO2 remained within normal physiologic limits. Simultaneous infusion of ritodrine (400 mug per minute) and propranolol (100 mug per minute) blocked the maternal tachycardia, but decreases in UtBF, MMAP, and UmBF were observed. Ritodrine infusions to the fetus (25 mug per minute) resulted in fetal tachycardia and a variable increase in UmBF.
OBJECTIVES: The purpose of this study was to determine whether continuous infusion of ritodrine could prevent preterm delivery in sheep. STUDY DESIGN: Sheep in preterm labor induced by RU 486 (mifepristone) received infusions of either ritodrine (n = 5) or saline solution (n = 5), and the progress of labor was monitored. beta 2-Adrenergic receptor density and function (agonist-induced cyclic adenosine monophosphate production) was measured in myometrial samples from both groups. RESULTS: Ritodrine initially inhibited labor contractions. This inhibition was only maintained for 16 hours, after which both the amplitude and frequency of electromyographic bursts and contractions returned. The failure of the myometrium to respond to ritodrine (desensitization) was associated with significant reductions in agonist-induced cyclic adenosine monophosphate production and beta 2-adrenergic receptor concentration in myometrial tissue collected from these animals compared with the saline solution-treated controls. CONCLUSIONS: Continuous infusion of ritodrine to sheep in preterm labor produces only a transient inhibition of contractions. This desensitization is caused by a down-regulation of myometrial beta 2-adrenergic receptors.
Twenty-nine women with premature labor were randomly assigned to a ritodrine (N = 14) or placebo (N = 15) drug group. The 2 groups were of similar age, parity, weight, gestational age, and cervical change at the onset of treatment. They were treated sequentially with intravenous, intramuscular, and oral drugs and monitored carefully during therapy. There was a significant increase in both the maternal and fetal heart rates during ritodrine treatment, and also a significant decrease in maternal blood pressure. Ritodrine-treated women often complained of palpatations. There was no significant difference in the extension of pregnancy, birth weight, or infant survival for the ritodrine group. Although the 1-minute Apgar scores in the ritodrine group were higher, the 5-minute scores were similar in both groups.
For a period of 8 days, pregnant white New Zealand rabbits were treated either with the beta-sympathomimetic Ritodrine (1 mg/kg) body weight daily) or with 0.9% saline solution. The fetuses were delivered by caesarian section on the 25th and 30th day of gestation (term being 31 days). No significant difference was found between the Ritodrine and saline treated groups with respect to the levels of dipalmitoyl-lecithin (DPL) obtained from the homogenates as well as the alveolar lavages of the fetal lungs. These results indicate that with this experimental model, prepartum treatment with Ritodrine has no effect either on DPL synthesis or its release into the alveolar spaces. Furthermore, treatment with the beta-sympathomimetic produced no significant change in the concentrations of the specific glucocorticoid receptors in the cytosol and nuclei of the fetal lungs, and in addition, the lung cytosol glucose concentrations as well as the plasma corticosteroid levels were unaffected. These findings support the conclusion that the synthesis of DPL in the fetal lung is not stimulated by Ritodrine.
Twenty-nine women in premature labor were randomly assigned to a ritodrine (N = 14) or placebo (N = 15) treatment group. Thirteen serial blood samples were drawn during the first 12 hours of therapy by intravenous drug infusion and they were analyzed for a variety of metabolic substances. There was a significant increase in the blood glucose level in the ritodrine group after one hour and this persisted for the 12 hours of intravenous drug treatment. Plasma insulin levels similarly did not increase in the placebo but significantly rose in the ritodrine group by 30 minutes, peaked at 2 1/2 hours, and remained elevated throughout the infusion. There were no significant differences between levels of plasma glucagon, cholesterol triglyceride, human placental lactogen, or human chorionic gonadotropin in the two treatment groups. Ritodrine caused significant maternal and fetal tachycardia. Its use in women with carbohydrate abnormalities should be monitored carefully. The increased glucose levels may lead to an increased fetal weight.
The changes in the maternal circulation following administration of ritodrine hydrochloride were investigated in chronically prepared pregnant sheep. Low infusion rates of ritodrine (see text) elevated the maternal heart rate and cardiac output and decreased peripheral vascular resistance. Stroke work fell while minute work increased. The distribution of uterine blood flow did not change, as measured with microspheres. Simultaneously measured fetal cardiac output and umbilical blood flow were not altered. When ritodrine infusion rates (see text) were increased there was a slight but significant decrease in uterine perfusion pressure, and an increase in uterine vascular resistance with uterine blood flow decreasing. These changes were observed when the ewes were not in labor, and similar changes were again recovered with ewes in labor despite the simultaneous inhibition of uterine contractions. Selective beta blockade with practolol during ritodrine administration decreased the maternal tachycardia without affecting cardiac output, peripheral vascular resistance, or uterine vascular resistance.
The effect of ritodrine hydrochloride on uterine blood flow was investigated in near-term guinea pigs. The infusion of ritodrine in doses sufficient to inhibit uterine activity provoked tachycardia, and the cardiac output tended to rise. The percentage of cardiac output reaching the gravid uterus did not alter during the infusion of 12 micrograms per minute of ritodrine but decreased from 12% to 10% when the infusion rate was 120 micrograms per minute. There was an increase in the myoendothelial fraction of cardiac output in both instances, whereas the placental fraction decreased at the higher rate of infusion. Perfusion of the myoendothelial tissue improved during the infusion of 12 or 120 micrograms per minute of ritodrine, increasing by 25% and 18% respectively. No significant alteration occurred in the perfusion of the placental tissue.
A prospective and double-blind study was undertaken to compare the effectiveness of two different treatments on two randomized groups of patients with threatened preterm labor. The first treatment consisted of the administration of ritodrine and a placebo; in the second, ritodrine was combined with indomethacin. 22 patients were evaluated in each group. The results obtained for gain in days, number of patients delivered at term, weight of newborns and number of recurrences in each group suggest that treatment with ritodrine and indomethacin is slightly but significantly more effective than treatment with ritodrine and placebo in prolonging pregnancy. No evidence has been found of possible unfavorable vascular effects of indomethacin in the fetus or the newborn.
The object of this double-blind crossover study was to investigate the effect of a beta-mimetic agent-ritodrine-administered intravenously at increasing infusion rates on uterine blood flow and the maternal cardiovascular system during the third trimester of normal pregnancies and pregnancies complicated by intrauterine growth retardation and/or hypertension. Uterine blood flow, maternal arterial blood pressure, maternal and fetal heart rate, and uterine activity were simultaneously recorded throughout the study. In normal pregnancies the changes in different parameters during ritodrine and placebo administration were slight. In the "pathologic" pregnancies there was a highly significant increase in maternal heart rate, differential blood pressure, and uterine blood flow during ritodrine administration. The differences in response to ritodrine and placebo were statistically significant in this later group. This study demonstrates increased sensitivity of the maternal cardiovascular system to this beta-mimetic agent in certain categories of high-risk pregnancies and possibily an increase in uteroplacental blood flow.
The perinatal mortality rate for twin gestation is in the range of 15%, and this is due predominantly to prematurity, although twins may also be born growth retarded. Ritodrine HCl, a beta sympathomimetic drug, has been shown to be effective, both in stopping premature labor and in preventing intrauterine growth retardation. With this in mind, a double-blind study using ritodrine HCl or placebo was begun in order to study its effect on premature labor, intrauterine growth retardation, and the perinatal mortality rate in twins. Thus far, 30 patients have delivered and have been followed to 6 weeks postpartum. Although the results on individual patients have remained blinded to the investigators, an initial evaluation of the ritodrine and placebo groups have revealed no difference with respect to gestational age, birth weight, or perinatal mortality. These preliminary results are not significant. However, it appears that ritodrine HCl is a safe oral agent for the antepartum gravida and her fetus. The study will be continued until approximately 100 patients have been enrolled.
beta-Adrenergic agents are used to inhibit preterm labor and glucocorticoids to accelerate fetal pulmonary maturation. A study was designed to investigate the metabolic effects of intravenous infusion of ritodrine (150 to 100 microgram/min) or isoxsuprine (200 to 150 microgram/min) in a series of 28 patients with gestations of 28 to 40 weeks, with and without concomitant dexamethasone therapy. Ritodrine was more potent than isoxsuprine in increasing the circulating levels of cyclic AMP, glucose, insulin, and triglycerides. The diabetogenic effect of both ritodrine and isoxsuprine was so slight that it did not have any clinical significance in women with normal glucose tolerance. The results were similar when these beta-adrenergic tocolytics were given to women concomitantly with intramuscular dexamethasone therapy, although dexamethasone appeared to minimally impair carbohydrate metabolism. Both ritodrine and isoxsuprine caused a significant fall in serum iron and potassium, and this effect was unaltered by dexamethasone. Serial serum potassium levels should be obtained during long-term infusion of beta-mimetics.
The effect of intravenous administration of ritodrine on blood glucose, insulin, free fatty acids and electrolytes in 17 third-trimester gravidas was investigated. A highly significant increase in blood glucose, insulin and free fatty acids and a marked decrease in serum potassium levels were registered. No significant changes during ritodrine infusion were recorded in serum levels of sodium, chloride, calcium, phosphorus and magnesium. No cardiac arrhythmias or electrocardiographic deteriorations occurred. While intravenous ritodrine administration seems to be safe in normal pregnancy, there may be a risk in diabetic patients, digitalized cases and those patients being treated with diuretics.
The reported growth-promoting effects of the beta-sympathomimetic compound, ritodrine, have been investigated. The carbohydrate tolerance of eight pregnant women was found to be unaffected by treatment with oral ritodrine over a ten-week period. A further observation that the carbohydrate metabolism of the newborn infants of these women was within normal limits tends to discount possibility that any growth-promoting action ritodrine may have on the fetus is mediated through a diabetogenic effect on the mother.
The effects of ritodrine infusion on the cardiovascular system of six women in threatened or premature labour are reported. In contrast to other betamimetics, ritodrine caused a moderate rise in systolic blood pressure, the corresponding fall in diastolic pressure leading to a widened pulse pressure but no risk of hypotension. Ritodrine caused a rise in cardiac output, and was well tolerated by the patients. Special care should be taken in treating patients with known heart disease.