Pharmacokinetics and Pharmacodynamics of Nifedipine in Patients at Steady State

Gutiérrez, Luis M.; Lesko, Lawrence J.; Whipps, R.; Carliner, Nathan H.; Fisher, Martin

doi:10.1002/j.1552-4604.1986.tb02954.x

Cited by 16 publications

(4 citation statements)

References 21 publications

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“…Although the pharmacokinetics and pharmacodynamics of nifedipine have been characterized extensively in adults (6)(7)(8)(9), only a few studies to date have evaluated the hemodynamic responses in a pediatric population (3)(4)(5), and pharmacokinetic studies in this population are completely lacking. The objectives of this study were to determine the pharmacokinetic properties of nifedipine in children with BPD and pulmonary artery hypertension after the administration of a single oral dose of the drug, and to evaluate the relationship between plasma nifedipine concentrations and the acute responses.…”

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confidence: 99%

Pharmacokinetics and Pharmacodynamics of Nifedipine in Children with Bronchopulmonary Dysplasia and Pulmonary Hypertension

et al. 1991

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ABSTRACT. The pharmacokinetics and associated pharmacodynamics of nifedipine were studied in nine children aged 5 to 68 mo with bronchopulmonary dysplasia and pulmonary artery hypertension after a single oral dose of 1.44 tLmol/kg (0.5 rug/kg). In the cardiac catheterization laboratory, hemodynamic measurements were made in duplicate just before the nifedipine dose and at 5 min and 0.5 and 1.0 h after the dose. The plasma nifedipine concentration was measured by HPLC at each of the above times and at 2.5, 4.0, 6.0, and 8.0 h after the dose. The mean (± SD) maximum plasma concentration and the time to maximum plasma concentration were 243.4 ± 194.5 nmol/L and 1.0 ± 0.8 h, respectively. The mean area under the plasma concentration-time curve was 761 ± 509 nmol-h/ L. The mean elimination rate constant and t,;, were 0.456 ± 0.194 h-I and 1.8 ± 0.8 h, respectively. Nifedipine caused a significant (p ::s 0.05) reduction in the mean pulmonary artery pressure by 5 min and in the mean pulmonary vascular resistance index and mean aortic pressure by 30 min, and these reductions remained significant through the J-h measurement interval. The magnitude of acute hemodynamic response correlated closely with the plasma nifedipine concentrations. No significant change occurred in the mean arterial oxygen saturation or cardiac index during the study period. The percentage changes from baseline in the mean pulmonary artery pressure and mean pulmonary vascular resistance index were approximately double the percentage change in the mean aortic pressure, suggesting that nifedipine had some degree of selective impact on the pulmonary vascular bed. Based on these results, an initial oral maintenance regimen of 1.44 tLmol/kg (0.5 mg/kg) every 6 h would be needed for this patient population. If the safety and efficacy after chronic therapy can also be shown, nifedipine may prove to be an important therapeutic addition to the management of children with bronchopulmonary dysplasia and pulmonary hypertension.

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confidence: 99%

Pharmacokinetics and Pharmacodynamics of Nifedipine in Children with Bronchopulmonary Dysplasia and Pulmonary Hypertension

et al. 1991

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“…in patients with angina pectoris (five with congestive HF, NYHA class I and II; five with hypertension) with no evidence of renal or hepatic impairment are not significantly different from those reported in healthy subjects [137]. The kinetics of oral nifedipine at steady state C 10-40 mg t.i.d.)…”

Section: Nifedipinementioning

confidence: 78%

Effects of cardiovascular disease on pharmacokinetics

Rodighiero

1989

Cardiovasc Drug Ther

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The pathophysiologic changes occurring in cardiovascular disease can affect the kinetics of drugs in several different ways. The present review examines these modifications and the underlying mechanisms. The kinetics of specific agents, such as antiarrhythmic, antihypertensive, cardiotonic, and other drugs are considered, and the clinical implications are outlined. The clinician should be aware of these modifications, because they require an adjustment of the dosage regimen. A rational basis for a correct therapeutic choice can be provided by adequate knowledge of these modifications.

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“…In order to imitate the serum condition of patients who take dihydropyridine, a concentration of 0.34 μ m nifedipine was added to the medium as a serum background agent in this study (20–22). In addition, 10 ng/mL of IL‐1β was applied to stimulate both healthy and DIGO human gingival fibroblasts (23).…”

Section: Methodsmentioning

confidence: 99%