Maternal and Fetal Metabolic Effects of Prolonged Ritodrine Infusion

Bassett, J. M.; Burks, A. H.; Levine, David H.; Pinches, Robert; Visser, G. H. A.

doi:10.1097/00132582-198606000-00003

Cited by 6 publications

(11 citation statements)

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“…In that situation, direct actions of ritodrine within the fetus would be additional to those resulting from altered placental nutrient fluxes caused by disturbances to maternal metabolic homeostasis in the early stages of drug administration. During our present investigation, there were no changes in maternal metabolism comparable to those observed during ritodrine administration to the ewe (5).…”

Section: Discussioncontrasting

confidence: 57%

“…Hematocrits were determined using a microhematocrit centrifuge (Hawksley, Sussex, UK). Blood glucose, lactate, and the hormones insulin and glucagon were determined by methods reported previously (5,6). FFA were determined on 100-pL samples of fetal plasma by a microcolorimetric method using Wako NEFA kits (Alpha Laboratories, Fareham, Hants, UK) after first diluting both the reagents to half the recommended concentration.…”

Section: Animals and Theirpreparationmentioning

confidence: 99%

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Desensitization of β-Receptor Mediated Responses to Epinephrine in Fetal Lambs by Prolonged Ritodrine Administration

1990

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ABSTRACT. During prolonged administration of @-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 wg/min), whereas blood Poz 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 pg/min i.v. for 60 min, then 2 pg/min i.v. for a further 60 min) was infused into fetal lambs (124-130 d gestation) 1 d before, then 5 f 1 d after, and again 10 f 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 f 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 @-adrenergic receDtor mechanisms were clearlv decreased when administration of @-agonists was prolonged beyond 24 h. (Pediatr Res 28: 388-393,1990) typical of prolonged stimulation of P-adrenergic receptor mechanisms. Hyperglycemia, hyperlactacidemia, and hyperinsulinemia occur and acid-base balance is severely taxed during the 1st 48-72 h of infusion. Further, Warburton et al. (7) have observed that the hyperglycemia is associated with substantial depletion of hepatic glycogen reserves after 24 h administration. Also, both we (6) and Warburton et al. (8) have shown that administration of ritodrine for 24 h or longer results in the development of marked hypoxemia at least as severe as that seen in fetal lambs during prolonged hyperglycemia and/or hyperinsulinemia (9, 10). After administration of the drug for more than 48 h, these changes moderate (6). It appears that it is only the development of tachyphylaxis to the drug that permits the restoration of homeostasis during more prolonged administration. Indeed, Warburton et al. (1 1, 12) have shown that there is already a very marked reduction in the P-adrenergic receptor population of fetal lung tissue after 24 h of ritodrine administration. More widespread changes in sensitivity of P-adrenergic receptor mechanisms have not been investigated.Although this reduction in sensitivity may permit fetal survival in the face of prolonged ritodrine treatment, we questioned whether it might have other less desira...

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Section: Discussioncontrasting

confidence: 57%

Section: Animals and Theirpreparationmentioning

confidence: 99%

Desensitization of β-Receptor Mediated Responses to Epinephrine in Fetal Lambs by Prolonged Ritodrine Administration

1990

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“…They suggest that there is a link between chronic beta adrenergic agonist use and PPCM, and advocate close evaluation of cardiac function of all pregnant women receiving long-term beta sympathomimetic tocolysis. In a series of 15 women on ritodrine tocolysis, 11 of them developed ECG changes consistent with myocardial ischaemia [94]. The authors postulate that silent ischaemia could contribute to the cardiomyopathy that has been reported after prolonged ritodrine treatment.…”

Section: Prolonged Tocolysis As a Risk Factormentioning

confidence: 99%

“…Prolonged tocolysis refers to the use of tocolytic agents for a period greater than four weeks [94]. Pulmonary oedema occurring in the peripartum period has long been associated with the administration of tocolytic drugs, which include terbutaline, ritodrine, salbutamol, isoxsuprine and magnesium sulphate [95].…”

Section: Prolonged Tocolysis As a Risk Factormentioning

confidence: 99%

Aetiology and risk factors of peripartum cardiomyopathy: A systematic review

Ntusi

Mayosi

2009

International Journal of Cardiology

136

105

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“…In 1979, ritodrine was acknowledged as safe and effi cient for the treatment of preterm labor [2], However, numerous maternal [2] and fetal [3] side effects have been attributed to the drug, which, due to its low molec ular weight, 287 dalton, was reported to cross the mater nofetal barrier [4] and to affect placental metabolism in vitro [5]. Ritodrine transfer across the placenta was pre viously studied in vivo in humans [4], However, accu rate transfer measurements were difficult to perform, and evidence for ritodrine accumulation in placental tis sue was not substantiated.…”

Section: Introductionmentioning

confidence: 99%

Transplacental Transfer of Ritodrine and Its Effect on Placental Glucose and Oxygen Consumption in an in vitro Human Placental Cotyledon Perfusion

Urbach

Mor²,

Fuchs³

et al. 1991

Gynecol Obstet Invest

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Maternofetal transfer of ritodrine and its effect on placental glucose and oxygen consumption were studied using a recycling perfusion of maternal and fetal circulations of an isolated cotyledon of a term human placenta, ³H-labeled ritodrine was introduced into the maternal side of the perfusion system. Transfer was calculated from the linear rise of ritodrine concentrations on the fetal side and was found to be 7.31 ± 1.02 ng/g placental wet weight/min (SEM) when 1.4 µg/ml of ritodrine was used (n = 3) and 14.7 ± 1.06 ng/g placental wet weight/min when the concentration was 2.8 µg/ml (n = 5). The antipyrine transfer rate, 4.1 ± 0.51 mg/kg/min (n = 8), was used to demonstrate perfusion adequacy and served as an internal standard. Upon computing the mass balance of ritodrine and antipyrine at the end of the experiment, it was found that 17% of ritodrine disappeared from the perfusion system compared to 0.7% of antipyrine (p < 0.01). The introduction of ritodrine into the perfusion system did not affect placental glucose and oxygen consumption rates of 0.35 ± 0.01 µmol/g/min (n = 7) and 0.19 ± 0.013 µmol/g/ min (n = 5), respectively.

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Maternal and Fetal Metabolic Effects of Prolonged Ritodrine Infusion

Cited by 6 publications

References 0 publications

Desensitization of β-Receptor Mediated Responses to Epinephrine in Fetal Lambs by Prolonged Ritodrine Administration

Desensitization of β-Receptor Mediated Responses to Epinephrine in Fetal Lambs by Prolonged Ritodrine Administration

Aetiology and risk factors of peripartum cardiomyopathy: A systematic review

Transplacental Transfer of Ritodrine and Its Effect on Placental Glucose and Oxygen Consumption in an in vitro Human Placental Cotyledon Perfusion

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