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PubMed2005

Inhibitory effects of various beverages on ritodrine sulfation by recombinant human sulfotransferase isoforms SULT1A1 and SULT1A3.

PURPOSE: Ritodrine is known to undergo extensive presystemic sulfation in the intestinal mucosa, and its bioavailability is as low as 30%. Accordingly, inhibition of intestinal sulfation may lead to an increase in the bioavailability of ritodrine. In this study, we aimed to investigate the activities of ritodrine sulfation by SULT1A1, which is expressed predominantly in the liver, and SULT1A3, which is expressed predominantly in the intestine, as well as the inhibitory effects of beverages on their activities. METHODS: We investigated ritodrine sulfation by using recombinant human sulfotransferase (SULT) 1A1 and SULT1A3 in an in vitro study. Next, we investigated the inhibitory effects of grapefruit juice, orange juice, green tea, and black tea on ritodrine sulfation. RESULTS: Sulfation of ritodrine by SULT1A3 was much higher than that by SULT1A1, suggesting that the bioavailability of ritodrine may be limited by intestinal SULT1A3. The ritodrine sulfation activities of SULT1A1 and SULT1A3 were significantly inhibited by all beverages examined at a concentration of 10%. Green tea and black tea exhibited potent inhibition; even at a concentration of 5%, they both inhibited SULT1A1 by 100% and SULT1A3 by >or=95%. CONCLUSION: Our results suggest that concomitant ingestion of beverages such as green tea and black tea may increase the bioavailability of orally administered ritodrine, and perhaps other beta2-agonists, and lead to an increase in the clinical effects or adverse reactions.

Adrenergic beta-Agonists↗
PubMed1988

Dexamethasone effects on ritodrine-induced changes in myometrial contractility and beta-adrenergic receptor function.

We have previously demonstrated in pregnant sheep that ritodrine infusion for 24 hours reduces myometrial beta-adrenergic receptor density and isoproterenol-stimulated adenylate cyclase activity. These receptor-associated changes were accompanied by an increasing inability of ritodrine to inhibit uterine contractility induced by a bolus of oxytocin. In the present study, we evaluated whether these ritodrine-induced effects could be altered by dexamethasone. Ten pregnant sheep at gestational ages of 92 to 130 days received ritodrine 2 micrograms/kg/min for 24 hours. Five animals also received dexamethasone 10 mg intravascularly twice during the ritodrine infusion. Before and at 4 and 24 hours of ritodrine infusion, the animals were given an identical dose of oxytocin as a bolus, and the area under the uterine pressure-time curve was quantified. Myometrial biopsy specimens were obtained before and after ritodrine infusion. Dexamethasone treatment prevented ritodrine-induced reductions in beta-adrenergic receptor density and isoproterenol-stimulated adenylate cyclase activity. Despite these receptor-associated effects, dexamethasone did not prevent the loss of tocolytic efficacy associated with prolonged ritodrine infusion.

Animals↗
PubMed1990

Pharmacokinetics and pharmacodynamics of ritodrine after intramuscular administration to pregnant women.

To define the pharmacokinetics and pharmacodynamics of ritodrine after intramuscular injection, we administered 5 or 10 mg ritodrine into the gluteus or deltoid muscles of 12 pregnant volunteers. Six women received 5 mg and six received 10 mg into each muscle group on different days. We withdrew blood samples before and 12 times in the 6 hours after ritodrine injection. Blood pressure and heart rate were recorded at each time. Ritodrine was measured by high-performance liquid chromatography. Peak ritodrine concentrations (mean +/- SD) after a single 5 mg injection in the deltoid or gluteus were 38 +/- 13 and 26 +/- 8 ng/ml, respectively. After a 10 mg dose in the deltoid or gluteus, peak concentrations were 59 +/- 30 and 47 +/- 22 ng/ml, respectively. Although higher, the peak plasma concentrations after injections into the deltoid were not significantly greater than those after injection into the gluteus. None of the pharmacokinetic parameters differed according to dose or injection site. The pharmacodynamic effects of ritodrine were unaffected by injection site, but ritodrine caused a dose-related increase in heart rate and systolic blood pressure and a dose-related decrease in diastolic blood pressure. After a 10 mg injection, the maximal changes in heart rate, systolic, and diastolic blood pressure were 22%, 10%, and 19%, respectively. However, mean blood pressure was not altered by either the 5 or 10 mg dose. These findings indicate that there are few differences in pharmacokinetic parameters between deltoid and gluteal injection of ritodrine. The single intramuscular injection of 5 or 10 mg ritodrine results in labor-inhibiting concentrations with clinically insignificant cardiovascular effects.

Arm↗
PubMed1991

Levels of ritodrine hydrochloride in fetal blood and amniotic fluid following long-term continuous administration in late pregnancy.

Placental transfer of ritodrine hydrochloride (ritodrine) was investigated in late-pregnant women following continuous infusion. Five volunteer women undergoing cesarean section received a total dose of 650-5970 mg of ritodrine for 8-49 days. After the infusion was discontinued at cesarean section, maternal and fetal blood and amniotic fluid were collected for later determinations of ritodrine by radioimmunoassay. Maternal serum concentrations of ritodrine were between 99.0-332.4 ng/ml. Serum levels of ritodrine in cord artery and vein were 75.9-250.5 ng/ml and 74.7-213.0 ng/ml, respectively. Ritodrine levels in amniotic fluid ranged from 126.0 to 424.0 ng/ml. The concentration of ritodrine in cord vein to maternal vein (CV/MV) was 0.695 +/- 0.066 (m +/- SE), while the concentration ratio of the amniotic fluid to maternal vein (AF/MV) was 1.719 +/- 0.211. In the present study of continuous administration of ritodrine, remarkably higher concentrations in fetal circulation and amniotic fluid were observed compared to those in cases of short-term infusion.

Abortion, Threatened↗
PubMed1984

Adjunctive use of magnesium sulfate with ritodrine for preterm labor tocolysis.

The purpose of the study was to determine if the adjunctive administration of magnesium sulfate with ritodrine would result in decreased dosage requirements of ritodrine, and, therefore, decrease the incidence of ritodrine-associated side effects. Candidates for tocolysis were prospectively randomized so that some received a uniform tocolytic dose of magnesium sulfate in a blinded protocol. All patients received a ritodrine infusion which was titrated in the standard manner to achieve cessation of labor. Evaluations included interval cumulative ritodrine dose, maximal ritodrine infusion rate, fluid balance, and blood chemistry studies. Contrary to our hypothesis, there were significantly more cardiovascular effects in the group that received ritodrine plus magnesium sulfate (11/24) than in the group that received ritodrine alone (1/17) (p less than or equal to 0.02). The predominant side effect was chest pain, frequently associated with electrocardiogram changes indicative of myocardial ischemia. These results are consistent with the current understanding of the regulatory mechanisms of these tocolytic agents. We conclude from the results of our prospective, randomized, blinded study that the adjunctive use of magnesium sulfate with ritodrine is associated with an unacceptable increase in serious side effects and probably does not improve efficacy.

Adult↗
PubMed1982

Effects of ritodrine, a beta 2-adrenoceptor agonist, on smooth muscle cells of the myometrium of pregnant rats.

1 Effects of ritodrine on the electrical and mechanical activities of the myometrium of pregnant rats were investigated in relation to cyclic adenosine 3',5'-monophosphate (cyclic AMP) production and the actions of isoprenaline. 2 In the longitudinal muscle cells of the 22nd day of gestation, ritodrine (greater than 10(-8) M) hyperpolarized the membrane, reduced the membrane resistance and suppressed the amplitude of contraction. Increased concentrations of ritodrine (greater than 10(-7) M) suppressed the generation of spikes and increased the amount of cyclic AMP produced. These actions of ritodrine were much the same as those of isoprenaline but the dose-response curves of all parameters were shifted to the right. 3 The effects of ritodrine on the circular muscle cells at the 22nd day of gestation were similar to those observed in the longitudinal muscle cells. 4 In the circular muscle cells at the 17-19th days of gestation, ritodrine produced neither a hyperpolarization nor an increase in cyclic AMP production (up to 10(-5) M) but did reduce the plateau potential and did relax the tissue (greater than 10(-7) M). 5 In the longitudinal muscle cells, during the 17-19th days of gestation, the responses of the tissues were similar to those observed in circular muscles on the 22nd day of gestation. These actions of ritodrine were suppressed by propranolol (10(-6) M). 6 These results indicate that ritodrine is a beta-adrenoceptor agonist and its mechanism of action similar to that of isoprenaline. However, the potency of ritodrine was approximately 100 times less than that of isoprenaline.

Animals↗
PubMed2005

Ritodrine in the treatment of preterm labour: a meta-analysis.

BACKGROUND & OBJECTIVES: Results on the effect of ritodrine in the treatment of preterm labour are different all over the world. Therefore, a concrete conclusion cannot be drawn from a single randomized control trial (RCT). In this study, we selected a large number of RCTs worldwide on the treatment of preterm labour comparing ritodrine and placebo or magnesium sulfate and by applying meta-analysis, evaluated the effect of ritodrine in the treatment of preterm labour. METHODS: We searched and identified 20 RCTs about ritodrine versus placebo, and ritodrine versus magnesium sulphate in the main medical data resources (MEDLINE, PubMed, CBMdisc, Cochrane Library and EMBASE) from January 1970 to December 2001 published in English and Chinese literature. We abstracted data about delay of gestation, gestational age at delivery, birth weight, severe neonatal respiratory system diseases, perinatal deaths, and administration to contraction-ceased interval, etc. RESULTS: The odds ratio (OR) of 1 day (d) delay in 10 RCTs on ritodrine in preterm labour versus placebo was 2.95 (95%CI 2.15, 4.04), and OR of 2d delay was 1.91 (95%CI 1.49, 2.45), both differences were statistically significant. There were no significant difference on the OR of birth > or =37 wk, birth weight > or =2500 g, severe respiratory morbidity and perinatal mortality. The OR of 2d delay of four RCTs from abroad on ritodrine versus magnesium sulphate was 1.56 (95%CI 0.62, 3.94), and OR of 7d delay was 1.45 (95%CI 0.80, 2.62), both without significant difference. But the combined estimated rate difference (CERD) of side effects interruption rate was 12 per cent with significant difference. There were six Chinese RCTs on ritodrine and magnesium sulphate. The OR of 1d delay was 3.95 (95%CI 1.98, 7.88), and OR of neonatal death was 0.45 (95%CI 0.22, 0.93), both with significant difference. The average administration to contractionceased interval were 2.5 and 6.3 h, respectively, with CERD being -4.2 h. INTERPRETATION & CONCLUSION: In treating preterm labour, ritodrine can significantly prolong a short interval more quickly but with relatively more side effects than magnesium sulphate. Stratified RCTs for different gestational ages and different labour stages should be designed for further study.

Adrenergic beta-Agonists↗
PubMed1992

Influence of a combination of ritodrine and nifedipine on the isolated rat uterus.

Studies were undertaken to evaluate the efficacy of the beta 2-adrenergic agonist ritodrine and the calcium channel blocker nifedipine, alone and in combination, for inhibition of contraction in isolated rat uterine strips. Both compounds produced a dose-dependent reduction of area under the curve. When contractions were produced by oxytocin, a 26% reduction was observed with 0.144mcg of ritodrine and a significant 68.1% decrease was produced with 1.44mcg of ritodrine. Contraction frequency (contractions per ten minutes) was not significantly affected. Prostaglandin F2 alpha-induced contractions were significantly inhibited 27.1% and 62.2% by 1.44mcg and 14.4mcg of ritodrine, respectively. Also, contraction frequency was significantly affected by both concentrations. Inhibition of area under the curve of oxytocin-induced contractions produced by nifedipine was 39.3% for 0.05mcg and 78.4% (P less than 0.05) for 0.50mcg. Contraction frequency was unaffected. Prostaglandin F2 alpha-induced contractions were significantly attenuated by 60% and 86% with nifedipine (0.50mcg and 5.02mcg, respectively); contraction frequency was significantly reduced from 15 to 2 contractions per ten minutes by 5.02mcg. Oxytocin-induced contraction was attenuated 39.8% by a combination of ritodrine 0.144mcg and nifedipine 0.05mcg; contraction frequency was unaffected. Area under the curve and contraction frequency of oxytocin-induced contractions were significantly decreased by a combination of ritodrine 0.144mcg and nifedipine 0.50mcg (89.8% reduction; decrease in frequency from 12 contractions in control to 4 contractions post-inhibitory agent). Significant attenuation of prostaglandin F2 alpha-induced contractions was produced by ritodrine 1.44mcg and nifedipine 0.50mcg. Area under the curve decreased by 73.2% and frequency was reduced from 13 to 8 contractions. A combination of ritodrine 1.44mcg and nifedipine 5.02mcg also produced significant decreases in area under the curve (85.3%) and frequency (13 contractions in control to 1 contraction after compounds were added). Because the mechanisms of action of these two agents are different, it is reasonable to suggest that they be used in combination to control premature labor. The results of this study suggest they may provide inhibition of contraction superior to either agent alone, and could therefore provide more effective inhibition and possibly reduce untoward side effects common to ritodrine therapy.

Animals↗
PubMed1991

Clearance and disposition of ritodrine in the fluid compartments of the fetal lamb during and after constant rate fetal intravenous infusion.

The disposition of the beta-2 adrenoreceptor agonist, ritodrine, has been examined in the fetal lamb during and after constant rate fetal intravenous infusion (8-24 h). Samples were collected from the fetal femoral artery, umbilical vein, maternal femoral artery, uterine vein, fetal trachea and the amniotic activity for ritodrine quantitation. The amniotic fluid was also analyzed for conjugated metabolites of ritodrine. Ritodrine appears to be cleared across the sheep placenta only to a limited extent (placental clearance 9.2 +/- 2 ml/min/kg; mean +/- S.E.M.). There is, however, significant fetal nonplacental clearance of ritodrine (fetal nonplacental clearance 52.8 +/- 8.0 ml/min/kg). At least part of this clearance appears to be due to fetal drug metabolism, as evidenced by the accumulation of glucuronide conjugates of ritodrine in the amniotic fluid. Ritodrine was also shown to accumulate in the amniotic and fetal tracheal fluids and persist after fetal arterial plasma ritodrine concentrations became undetectable. The accumulation of ritodrine in the tracheal fluid may be of pharmacologic significance, given the well documented, potent effects of beta-2 agonists on fetal lung function and development.

Animals↗
PubMed1989

[Pharmacokinetics and materno-fetal influence of ritodrine hydrochloride during the continuous treatment of threatened premature labor].

The cardiovascular and metabolic effects of ritodrine hydrochloride on the mother and fetus were investigated during the 28-day and/or longer continuous treatment of threatened premature labor. Concentrations of ritodrine in maternal venous blood during the treatment, and placental transfer of the drug into the fetal circulation and amniotic fluid were also determined to ascertain the effectiveness and safety of the drug. Seventeen volunteer patients at 27-34 weeks of gestation were given a total dose of 2,850-7,350mg of ritodrine intravenously at a mean infusion rate of 72.9 micrograms/min for 28-66 days, when the maternal serum concentration of ritodrine was maintained at approximately 200ng/ml throughout the treatment period. A significant but slight increase in the maternal heart rate and serum glucose, and a slight fall in maternal blood pressure were observed during ritodrine infusion. The fetal heart rate did not change significantly. Although ritodrine also produced decreases in the red blood cell count, hemoglobin and hematocrit, these changes were transient and recovered to the control level thereafter. The ratios of umbilical venous blood and the amniotic fluid concentration of ritodrine to maternal venous concentrations determined at cesarean section were 0.68 and 1.64, respectively, suggesting that a gradual accumulation of placentally transferred ritodrine may occur when long-term continuous infusion is carried out. There were no noticeable drug-related findings in mothers and newborns during and after labor. These results indicate that threatened premature labor may be well effectively controlled by ritodrine without severe side-effects on the mother or fetus in treatment for along period.

Adult↗
PubMed1985

Maternal and fetal plasma concentrations of ritodrine.

Previous studies using other beta-adrenergic drugs for tocolysis suggest that if treatment fails and the patient delivers shortly after the therapy is discontinued, there is a direct correlation between neonatal drug concentration and major neonatal complications. In the present study, the disposition of ritodrine was studied in 28 maternal-infant pairs in whom intravenous ritodrine had been administered for clinical indications. The fetal to maternal ratio of ritodrine was 1.17 +/- 0.48. The concentration of ritodrine in both maternal and umbilical vein was found to vary inversely with the length of time the drug was discontinued before delivery. A stepwise multilinear regression revealed that the maternal ritodrine dose in the 24 hours before delivery and the drug discontinuance to delivery interval were both independently related to umbilical vein ritodrine concentrations. When combined, the two variables explained 52% of the variance in umbilical vein ritodrine levels. The frequency of respiratory distress syndrome was increased in the neonates in whom umbilical vein ritodrine was greater than 10 ng/mL, compared with the groups with umbilical vein levels ranging from 3.0 to 10.0 ng/mL. However, neonates with the highest ritodrine concentration were also of lower gestational age (29.4 versus 33.5 weeks, P less than .05) and thus, had greater inherent risk of prematurity-related complications.

Chromatography, High Pressure Liquid↗
PubMed1997

Hyperamylasemia in response to ritodrine or ephedrine administered to pregnant women.

BACKGROUND: Ritodrine and ephedrine can induce hyperamylasemia in pregnant women. The incidence of these beta-agonist-induced hyperamylasemias and their interaction on serum amylase activity are not known. STUDY DESIGN: Serum amylase activity was determined 12 to 24 hours after the administration of ritodrine alone (n = 140), ephedrine alone (n = 160), ephedrine and ritodrine simultaneously (n = 34), and ephedrine after prolonged (> or = 7 days) use of ritodrine (n = 101). RESULTS: A significantly higher incidence of hyperamylasemia (amylase > 215 IU/L) was seen in a group treated with ritodrine alone (60/140, 43 percent), ephedrine alone (54/160, 34 percent), or ephedrine plus ritodrine (24/34, 71 percent) compared with untreated pregnant women (21/426, 4.9 percent). There was no difference in the incidence of hyperamylasemia among the untreated pregnant women and women who received ephedrine after long-term ritodrine (8/101, 7.9 percent). Isozyme patterns, examined in 72 out of the 146 women with hyperamylasemia after such medications, indicated that salivary-type amylase exclusively was hypersecreted. CONCLUSIONS: Clinical doses of beta-agonists such as ephedrine or ritodrine induce hypersecretion of salivary-type amylase in approximately one-third of women who are pregnant. Desensitization to beta-agonists may occur after prolonged use of ritodrine.

Adolescent↗
PubMed1983

Pharmacodynamics of ritodrine in pregnant women during preterm labor.

We evaluated the relationship of ritodrine concentration to several maternal variables and to fetal heart rate in 17 women who received the drug for inhibition of preterm labor. Ritodrine was measured by high-performance liquid chromatography with electrochemical detection. Ritodrine increased maternal and fetal heart rate and decreased serum potassium in a dose-related manner, but wide variability was noted between patients and within individual patients. Tachyphylaxis of the maternal heart rate response to continuing treatment with ritodrine was seen in at least seven women. Maternal blood pressure, serum glucose concentration, and frequency of uterine contractions were changed by ritodrine treatment, but the changes in these variables were not closely correlated to the concentration of ritodrine (r less than or equal to 0.30 in all cases). The maximal infusion rate and the concentration of ritodrine in maternal serum after 4 hours of treatment were significantly (p less than 0.001) correlated with the frequency of uterine contractions prior to treatment. Successful inhibition of labor was achieved with serum concentrations of 15 to 31 ng/ml in 10 of 17 women; in six of the other seven women, labor could not be inhibited in spite of serum concentrations of 90 to 146 ng/ml. Side effects, such as hypotension, vomiting, chest discomfort, and shortness of breath, were most commonly observed when the infusion rate and concentration of ritodrine were increasing.

Blood Pressure↗
PubMed1985

Evaluation of the pharmacodynamics and pharmacokinetics of ritodrine when administered as a loading dose. On establishing a potentially useful drug administration regimen in cases of fetal distress.

Inhibition of labor during the intrapartum period has been suggested as a method of managing acute fetal distress. In such cases, rapid tocolysis is desirable but, in high doses, beta-adrenergic-receptor agonists, such as ritodrine, may cause severe maternal hypotension that could aggravate the existing fetal distress. We undertook the present study to establish a safe infusion protocol for ritodrine that achieves high plasma concentration rapidly. Twelve nonpregnant female volunteers received, on separate days, three infusions of ritodrine, that is, 1, 2, and 3 mg, during a 2-minute period. The peak plasma concentration measured by high-performance liquid chromatography with electrochemical detection averaged 37, 74, and 100 ng/ml after the 1, 2, and 3 mg doses, respectively. Ritodrine concentrations decreased rapidly and with the 3 mg dose the ritodrine concentration was only 14 ng/ml after 15 minutes. The elimination phase half-life of ritodrine averaged 6.11 hours. None of the doses significantly affected systolic blood pressure but ritodrine increased heart rate and the plasma glucose level and decreased diastolic blood pressure and the plasma potassium concentration. Even at the highest infusion rate, the maximal changes in cardiovascular and metabolic variables were short-lived and clinically modest; heart rate increased 29 bpm, diastolic blood pressure decreased 8 mm Hg, glucose level increased 26 mg/dl, and potassium concentration decreased 0.6 mEq/L. These data indicate that high plasma concentrations of ritodrine can be achieved rapidly without serious side effects.

Adult↗
PubMed1986

Ventricular septal thickness and cardiac function in neonates after in utero ritodrine exposure.

Cardiac septal hypertrophy occurs after in utero ritodrine exposure. To assess the effect of septal hypertrophy on cardiac function we obtained M-mode echocardiograms on day 1 of life in 41 infants exposed to ritodrine and 22 control infants matched for gestational age. Mean duration of ritodrine exposure was 16.2 +/- 13.2 days (range 1 to 49 days). Disproportionate septal hypertrophy (DSH) was defined as an interventricular septal thickness/posterior wall thickness ratio (ST/PW) of greater than 1.3. Infants exposed to ritodrine in utero had DSH and increased right systolic time intervals compared with control values (P less than 0.05). A subgroup, those infants exposed for 2 weeks or longer, had not only DSH but also an absolute increase in septal thickness compared with control infants and infants exposed to ritodrine for less than 2 weeks. ST/PW correlated well with the duration of ritodrine exposure (r = 0.96); the longer the exposure the thicker the septum. Although all echocardiographic changes lasted for less than 3 months, we have no information regarding the effect on the fetus of maternal ritodrine exposure for longer than 7 weeks. Until such information is available, cardiac evaluation is recommended in neonates exposed to ritodrine in utero for longer than 7 weeks.

Cardiomyopathy, Hypertrophic↗
PubMed1992

Treatment of preterm labor with the beta-adrenergic agonist ritodrine.

BACKGROUND: Beta-adrenergic agonists are commonly used to arrest premature labor. Although treatment of preterm labor with these agents can delay delivery by 24 to 48 hours, the potential risks and benefits to the mother and infant before and after delivery have not been adequately assessed. METHODS: We randomly assigned 708 women with preterm labor at six hospitals to receive an intravenous infusion of either the beta-adrenergic agonist ritodrine (n = 352) or placebo (n = 356). Assignment was made with stratification according to four categories of gestational age (20 to 23 weeks, 24 to 27 weeks, 28 to 31 weeks, and 32 to 35 weeks). The primary objective was to assess the effect of ritodrine on perinatal mortality. Secondary objectives were the evaluation of the causes of perinatal death, the extent to which delivery was delayed with ritodrine, and the effects on birth weight, maternal morbidity, neonatal morbidity, and infant morbidity at 18 months of postnatal age, corrected for preterm delivery. RESULTS: Among the 771 infants born to the women in the study (including 63 pairs of twins), there were 23 deaths (6.1 percent) in the ritodrine group and 25 deaths (6.4 percent) in the placebo group (event-rate difference, -0.3 percent; 95 percent confidence interval, -3.7 percent to 3.1 percent). There was no difference between the groups in the extent of delay of delivery, the incidence of delivery before 37 weeks' gestation, the proportion of babies weighing less than 2500 g, or measures of neonatal morbidity. Maternal morbidity (such as chest pain and cardiac arrhythmias) occurred more frequently but not exclusively in the ritodrine group. One infant born to a woman in the ritodrine group and five infants born to women in the placebo group had cerebral palsy (P = 0.09). There was a slight but not significant trend toward an improved score on the Bayley Psychomotor Development Index at 18 months of age among the infants of the ritodrine-treated women. CONCLUSIONS: We found that the use of ritodrine in the treatment of preterm labor had no significant beneficial effect on perinatal mortality, the frequency of prolongation of pregnancy to term, or birth weight.

Birth Weight↗
PubMed1990

Desensitization of beta-receptor mediated responses to epinephrine in fetal lambs by prolonged ritodrine administration.

During prolonged administration of beta-agonists such as ritodrine directly to chronically cannulated fetal lambs, the cardiovascular, metabolic, and endocrine changes observed during the 1st day of administration, lessen and return to normal within 3-4 d despite continuing drug administration. In our investigation, heart rate, plasma FFA, lactate, glucose, and insulin concentrations all increased significantly during the 1st day of ritodrine infusion (10 micrograms/min), whereas blood PO2 and base excess were significantly decreased. After 3 d, despite continued drug infusion, all these changes had ameliorated. To examine the hypothesis that this tachyphylaxis to ritodrine also results in decreased sensitivity to endogenous catecholamines, epinephrine (1 microgram/min i.v. for 60 min, then 2 micrograms/min i.v. for a further 60 min) was infused into fetal lambs (124-130 d gestation) 1 d before, then 5 +/- 1 d after, and again 10 +/- 1 d after beginning ritodrine infusion. Before ritodrine administration, epinephrine significantly increased plasma FFA, lactate, glucose, and glucagon concentrations and decreased insulin. However, after ritodrine treatment for either 5 +/- 1 or 10 +/- 1 d, epinephrine resulted in no significant increases in FFA or glucagon, and those in lactate and glucose were significantly reduced. Decreases in insulin during epinephrine administration were unchanged by ritodrine. Initial responses of mean arterial pressure and heart rate to epinephrine were significantly greater during prolonged ritodrine treatment. Fetal responses to epinephrine mediated through beta-adrenergic receptor mechanisms were clearly decreased when administration of beta-agonists was prolonged beyond 24 h.

Animals↗
PubMed1984

Pharmacological investigation of ritodrine hydrochloride, a beta 2-adrenoceptor stimulant.

Ritodrine hydrochloride (ritodrine) has been effectively prescribed for the prevention of premature labor. The present study was carried out to investigate the mode of action of ritodrine on the uterus and heart in comparison with those of isoxsuprine and isoproterenol. 1) Ritodrine (10(-8)-10(-6) M) suppressed the spontaneous motility of pregnant rat uterus and showed positive chronotropic action at the doses of 10(-6)-10(-4) M in guinea-pig atria. 2) In the Ca2+-free, K+-rich Tyrode solution, ritodrine suppressed the Ca2+ induced contracture of pregnant rat uterus, while it potentiated the carbachol induced contraction. 3) Ritodrine increased the amount of cyclic AMP in the uterus but not in heart. This action of ritodrine was suppressed by pretreatment with propranolol (10(-6) M). 4) These results suggest that ritodrine causes actions through activation of cyclic AMP production, as in the case of isoproterenol, and it acts more selectively on beta 2-adrenoceptors than on beta 1-adrenoceptors.

Adrenergic beta-Agonists↗