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Biomedical subjects

P Lundborg

Publications and source records attributed to P Lundborg.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

The effect of antacid, metoclopramide, and propantheline on the bioavailability of metoprolol and atenolol.

Concomitant administration of antacid increased the maximum concentration (Cpmax) and the area under the plasma concentration-time curve (AUC) of 100 mg oral dose of metoprolol by 25 per cent (p less than 0.05) and 11 per cent (p less than 0.1) respectively. For atenolol the opposite effect was observed and Cpmax and AUC were decreased by 37 and 33 per cent respectively (p less than 0.02). In both cases the antacid did not affect the time-course of atenolol in the plasma or its bioavailability. Propantheline prolonged the absorption phase of atenolol and the time of peaking (tmax) was shifted from 2.1 to 4.5 h. Cpmax of atenolol was essentially unchanged by propantheline pretreatment while the AUC was increased by 36 per cent. It is concluded that the negative effect of the antacid on the bioavailability of atenolol is caused by a reduction in the in vivo dissolution rate due to increased gastric pH. The positive effect of propantheline might be due either to more efficient absorption of atenolol in the upper part of the intestine or more extensive dissolution of the drug as a result of prolonged contact with gastric juice or a combination of these factors.

Adult↗
PubMedDate not supplied

Pharmacokinetic and pharmacodynamic studies of felodipine in healthy subjects after various single, oral and intravenous doses.

The objective of this single-dose study was to evaluate the pharmacokinetics and haemodynamic changes in healthy male subjects following the administration of three oral (5, 15, and 40 mg) and two intravenous (1 and 3 mg) doses of felodipine, a new calcium antagonist with a selective effect on the peripheral resistance vessels. Felodipine was rapidly absorbed within 1 h when administered as an oral solution, but underwent extensive presystemic elimination. The systemic availability varied between 10 and 23 per cent. The disposition was adequately described by a two-compartment model: the disposition was essentially dose-independent up to 40 mg orally and 3 mg intravenously. Felodipine produced significant dose-dependent reduction of diastolic blood pressure and a significant reflexogenic increase in heart rate, without having any major effect on systolic blood pressure. These changes indicate that felodipine acts predominantly as an arteriodilator. The decrease in diastolic blood pressure and increase in heart rate were closely correlated with the plasma concentrations of unchanged felodipine, being maximal at 0.5 h and lasting for at least 4 h after the highest dose.

Administration, Oral↗
PubMedDate not supplied

Interaction in healthy volunteers between prenalterol, a selective beta 1-adrenoceptor agonist, and metoprolol or propranolol.

We studied the hemodynamic effects of the selective beta 1-adrenoceptor agonist prenalterol in healthy subjects before and after intravenous infusion of the nonselective beta-adrenoceptor blocker propranolol or the beta 1-selective adrenoceptor blocker metoprolol. Intravenous infusions of 0.1, 0.25, and 0.5 mg prenalterol induced a dose-dependent decrease in total electromechanical systole and pre-injection period, whereas left ventricular ejection time remained unchanged. Stoke volume as determined by impedance cardiography was not changed, but a dose-dependent increase in cardiac output due to an increase in heart rate was observed. Systolic blood pressure was significantly increased, but diastolic blood pressure remained unchanged. After intravenous administration of either 10 mg propranolol or 20 mg metoprolol, prenalterol was infused in a 10 times higher dose than before. The hemodynamic effects were similar to those observed before the beta-blockers. Whether propranolol or metoprolol was administered did not influence the effects induced by prenalterol. It is suggested that prenalterol might be a useful drug to counteract undesired hemodynamic effects of beta-adrenoceptor blockers.

Adrenergic beta-Agonists↗