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PubMedDate not supplied

Bioavailability of sustained release propranolol formulations.

In this comparative bioavailability study two sustained release capsule formulations of propranolol, one a clinical trial formulation and the other the U.K. sales formulation ('Inderal' LA), were compared with a conventional 'Inderal' tablet. Twelve healthy adult male volunteers received, on cross-over basis, on three separate occasions, 160 mg oral doses of three formulations of 'Inderal'. Bioavailability was based on concentration of propranolol in whole blood. The peak blood level and area under the propranolol blood level curve fell as the dissolution time increased. The half-lives of the three formulations were inversely proportional to their dissolution rates, those of the sustained release formulations being considerably longer than that of the conventional tablet. The 160 mg 'Inderal' tablet produced a rapid 90-fold decline over 24 h in propranolol blood levels following a high initial peak. By comparison both sustained release formulations showed a less rapid fall in systemic levels and gave higher blood levels at the end of 24 h and plateau values between 8 and 14 ng ml-1. The 'Inderal' LA sustained release formulation gave consistently higher propranolol blood levels than the clinical trial sustained release formulation. This result is in good agreement with their dissolution profiles. The lowering of the systemic bioavailability as the dissolution time increases is thought to be due to an increased metabolism of propranolol.

Adult↗
PubMed1995

Effects of sensory (teasing) exposure to food on oral propranolol bioavailability.

In order to further examine the mechanism of the increase in the plasma propranolol concentration versus time curve (AUC) caused by ingestion of propranolol with food, we administered R, S-propranolol tablets (0.5 mg kg-1) orally to healthy human volunteers and dogs in the presence and absence of sensory exposure to food without ingestion (teasing). Six healthy human volunteers were fasted on one occasion and on the other they were presented with an appetising meal, without eating it (teasing protocol). There was a strong trend to a greater propranolol AUC in the teasing protocol (139 +/- 54 mg mL-1 h-1 fasting, 178 +/- 105 mg mL-1 h-1 teasing; p = 0.1), and time of peak concentration (tmax) was significantly prolonged (80 +/- 22 min and 120 +/- 32 min, respectively; p < 0.03). Further studies were carried out in dogs who received R-propranolol (2 mg kg-1) as an oral solution by gavage tube on four different occasions: fasting, following intragastric administration of a high-value liquid meal, following teasing with food in the animal house at normal feeding time (high-intensity teasing). There were no significant differences in pharmacokinetic parameters between the fasting and intragastric food protocols. Low-intensity teasing resulted in significantly lower AUC and peak concentrations (Cmax) compared with fasting (p < 0.05), confirming food effect patterns known to occur in dogs. High-intensity teasing resulted in significantly greater AUC and Cmax compared with fasting (p < 0.05), reproducing in dogs the increase in propranolol AUC known to occur with food ingestion in humans. These findings suggest that the mechanism of the 'food effect' may involve physiological responses to the sight and smell of food additional to mechanisms activated by ingestion.

Administration, Oral↗
PubMed2003

Comparative pharmacokinetics and pharmacodynamics of propranolol and atenolol in normolipaemic and hyperlipidaemic obese subjects.

The lipophilic beta-adrenoreceptor antagonist propranolol and hydrophilic atenolol have been studied to define their pharmacokinetic and pharmacodynamic characteristics in obese patients. A total of 43 subjects were allocated into three study groups: (1) healthy, lean, normolipaemic volunteers, (2) obese normolipaemic subjects, and (3) obese patients with lipid disorders. A crossover method with an interval of 2 weeks was applied for oral 80 mg propranolol and oral 100 mg atenolol administration. Heart rate as well as systolic and diastolic blood pressure were recorded during 24 h. At each time-point of measurement blood serum concentration of propranolol and atenolol were evaluated. Pharmacokinetic parameters of the drugs were calculated using a one-compartment open model for extravascular administration. There were no statistically significant differences in blood serum concentrations of propranolol between the studied groups. The concentrations of atenolol were significantly lower in both normolipaemic and hyperlipidaemic obese subjects. A trend towards increase in Vd/F and Cl/F of propranolol in obese patients with hyperlipidaemia were noted. In the case of water-soluble atenolol, the AUC, C(max), Cl/(F x BW) were significantly lower in obese hyperlipidaemic and normolipaemic patients in comparison with lean subjects. The pharmacodynamic effects of propranolol and atenolol in obese and lean subjects were of similar magnitude. The observed differences between obese and non-obese persons were clinically not relevant.

Administration, Oral↗
PubMedDate not supplied

Steady state relative bioavailability and pharmacokinetics of oral propranolol in black and white North Americans.

The steady state bioavailability and pharmacokinetics of propranolol over two consecutive dosing intervals were investigated in 18 black and 10 white normal volunteers following the administration of 20 mg of a test and reference oral dosage form, respectively, every 6 h. There were no differences (p greater than 0.05) between dosage forms in the mean (n = 28) area under the plasma concentration-time curve (AUC), maximum plasma concentration (Cmax) or time to Cmax (tmax) for propranolol or its active metabolite, 4-hydroxypropranolol. However, as a group blacks had lower plasma concentrations of propranolol during the second dosing interval (AUC-2 and Cmax-2, respectively) were significantly (p less than 0.05) lower in blacks, but there were no ethnic differences (p greater than 0.05) in tmax. The mean AUC and Cmax for the 4-hydroxylated metabolite during both dosing intervals were significantly (p less than 0.05) lower in blacks. Mean oral clearances of propranolol, assuming complete absorption, (range: 42.1-54.5 ml min-1 kg-1) were similar (p greater than 0.05) in each racial group. There were no substantial changes in heart rate or blood pressure in blacks or whites following propranolol administration. These data suggest that for oral propranolol, blacks have different absorption and disposition characteristics than whites.

Administration, Oral↗
PubMed1982

Propranolol effects on autonomic function in hypertensive men.

Beta blocker antihypertensive effects are incompletely understood, and may involve alterations in the autonomic nervous system. We studied autonomic function in 12 essential hypertensive men during treatment with placebo and chronic oral propranolol. Propranolol reduced blood pressure and heart rate (both p less than 0.01) with an associated increase in baroreflex sensitivity during phenylephrine testing (p less than 0.02), though amyl nitrite-tested baroreflex sensitivity was unchanged; blood pressure decrement did not correlate with baroreflex enhancement. Response to the cold pressor test and the blood pressure decrement to phentolamine alpha blockade were unaltered by propranolol, suggesting unchanged efferent sympathetic function; nor were several biochemical indices of sympathetic nervous activity influenced by propranolol. Propranolol does perturb autonomic function in man, but the perturbations do not correlate with blood pressure decrement; nor are physiologic or biochemical indices of efferent sympathetic activity reduced by propranolol.

Adult↗
PubMed1975

Comparative effects of tolamolol and propranolol on cardiac and peripheral circulatory function in patients with coronary artery disease.

In a clinical study comparing the cardiocirculatroy effects of intravenous tolamolol to those of propranolol, tolamolol, 16 mg, induced similar reduction in resting heart rate as 8 mg propranolol in 16 coronary patients. Tolamolol did not disturb cardiac pump performance and exerted less negative inotropic action than propranolol as assessed by mechanical contractility indices. Myocardial beta-one chronotropic and inotropic stimulation by exogenous epinephrine was blocked equally by tolamolol and propranolol. Tolamolol exerted less systemic vascular beta-two blockade than propranolol as assessed by the peripheral resistance and vasopressor responses to epinephrine infusion. Tolamolction than propranolol and is thereby suitable for careful extension of beta blockade therapy to certain patients with pulmonary and ventricular dysfunction.

Adult↗
PubMed1976

Antihypertensive effects of oxprenolol and propranolol.

The antihypertensive effects of the beta blockers oxprenolol and propranolol were compared in a randomized double-blind study of patients with standing diastolic pressures (SDP) exceeding 99 mm Hg when receiving hydrochlorothiazide alone. After 3 wk of hydrochlorthiazide with placebo, the latter was replaced with oxprenolol (n= 12) or propranolol (n = 14), 20 mg three times daily. Beta blocker was increased subsequently to 40 and 80 mg three times daily if SDP exceeded 89 mm Hg. Nine oxprenolol and 7 propranolol subjects were hospitalized for 24-hr monitoring. With oxprenolol, standing pressure declined from 135 +/- 2 (SE)/104 +/- 1 MM Hg to 128 +/- 3/90 +/- 2. SDP declined to under 91 mm Hg in 7 of 12 subjects, and to from 91 to 95 in 3 subjects. With propranolol, findings were 138 +/- 3/106 +/- 2 to 123 +/- 3/89 +/- 3; in 7 of 12 to less than 91 mm Hg and from 91 to 95 in 4 subjects. Decrements in supine and SDP were slightly (4 mm Hg) greater for propranolol than for oxprenolol. Both drugs gave similar 24-hr blood pressure control. We conclude that oxprenolol and propranolol used to supplement hydrochlorothiazide provide comparable reductions in blood pressure and smooth control over a 24-hr period in most patients with hypertension.

Adult↗
PubMed1977

Oral and intravenous propranolol during exercise.

The intrinsic sinoatrial (SA) rate at rest and during exercise was measured in 5 normal male subjects after prolonged oral and acute intravenous administration of propranolol and atropine. At rest, the intrinsic SA rate was similar after both oral and intravenous propranolol. At the higher levels of power output on a cycle ergometer, cardiac rate was slower after oral than after intravenous propranolol. When the intravenous study was repeated with the use of an additional dose of propranolol, cardiac rate was lower at comparable levels of power output, but not as low as that after oral propanolol. Differences in responses were interpreted as reflecting varying degrees of beta blockade, the most complete being that after prolonged oral propranolol administration of 320 mg daily. The intravenous dose of propranolol usually used to obtain the "pharmacologically isolated heart" at rest is too small to induce full beta blockade in exercise.

Administration, Oral↗
PubMed1979

Effect of d- and dl-propranolol on glucose-stimulated insulin release.

The effect of intravenous d- and dl-propranolol on serum insulin levels has been examined before and after the administration of glucose orally to 10 normal subjects. The increase in serum insulin 45 to 90 min after glucose ingestion was reduced during the infusion of either d- or dl-propranolol. The insulin suppression was not accompanied by any alteration in the glucose curves. The insulin/glucose ratios were reduced by both d- and dl-propranolol during the time of maximum glucose and insulin responses. Neither d- nor dl-propranolol induced any significant change in basal glucose or insulin levels before glucose administration. Since d-propranolol has no appreciable beta adrenoceptor blocking activity, it appears that the suppression of glucose-stimulated insulin release by propranolol may be due primarily to local anesthetic properties which are exerted equally by both isomers.

Adult↗
PubMedDate not supplied

The developing liver: the steady-state disposition of propranolol in pregnant sheep.

The steady-state disposition of the beta-adrenoreceptor blocking drug, propranolol, and its metabolite, 4-hydroxypropranolol, was studied in the anesthetized pregnant sheep near term. Following infusion of propranolol to the mother, steady-state plasma concentrations were obtained at three dosage levels in each of the eight animals studied. Blood samples were obtained from : (i) maternal facial artery and hepatic vein; (ii) umbilical vein, and (iii) fetal carotid artery, portal vein, and right hepatic vein. Although total propranolol concentrations in maternal plasma were different from those in umbilical venous plasma, the concentrations of unbound drug were similar, suggesting that unbound drug had equilibrated across the placenta. Approximately 10% of propranolol was unbound in maternal plasma, compared with 30% in fetal plasma. Hepatic extraction of propranolol by the maternal liver was high, so that only 3 to 4% of the drug presented to the liver escaped uptake. In contrast, fetal hepatic extraction was low. Negligible amounts were removed from portal vein blood (right lobe), although one third was extracted from umbilical vein blood (left lobe). Mean peripheral arterial concentrations of 4-hydroxypropranolol were 2- to 3-fold higher in the fetus than in the mother. We conclude that the fetus is exposed to significant concentrations of propranolol and that the fetal hepatic extraction of this drug is considerably less efficient than in the adult. In contrast to the adult liver, the fetal liver does not appear to act as a single homogeneous organ, but rather as two distinct subunits.

Animals↗
PubMedDate not supplied

A carrier-protein receptor is not a prerequisite for avid hepatic elimination of highly bound compounds: a study of propranolol elimination by the isolated perfused rat liver.

The highly efficient hepatic extraction of propranolol by the isolated perfused rat liver does not diminish when albumin binding is increased from 30 to 75%. One possible explanation of this insensitivity of propranolol uptake to changes in albumin binding is the mediation of uptake of bound ligand by an albumin receptor on the hepatocyte as postulated for oleate, taurocholic acid and rose bengal. To test this hypothesis, the hepatic extraction of propranolol was studied in the isolated perfused rat liver using alpha 1-acid glycoprotein, which lacks a hepatocyte receptor, as the carrier protein in the perfusate rather than albumin. Livers were perfused with a medium containing propranolol (4 microM) and varying concentrations of alpha 1-acid glycoprotein (0 to 25 microM). Hepatic extraction of propranolol was very high (0.990 +/- 0.006; mean +/- S.D.) and did not alter significantly despite an increase in bound fraction from 0.2 to 0.8, thus closely paralleling the findings when albumin is the carrier protein. This result indicates that bound propranolol is efficiently cleared by the liver, presumably by a "free intermediate" mechanism, in the absence of a specific carrier-protein receptor on the hepatocyte. This study does not, therefore, support the albumin receptor hypothesis.

Albumins↗
PubMedDate not supplied

Prevention of recurrent bleeding in cirrhotics with recent variceal hemorrhage: prospective, randomized comparison of propranolol and sclerotherapy.

To compare the efficacy of endoscopic paravariceal sclerotherapy and oral propranolol in the prevention of recurrent upper gastrointestinal bleeding, 78 cirrhotic patients were randomly assigned to either treatment after an endoscopically proven bleed from esophageal varices. After randomization, but before treatment had been started, a total of eight patients had to be withdrawn from the study due to early rebleeding (requiring emergency sclerotherapy) or violations of the protocol. Among the 70 patients analyzed (36 sclerotherapy, 34 propranolol), both treatment groups were comparable with respect to demographic, clinical and laboratory data. The groups also did not differ with respect to continued alcohol intake. Sclerotherapy was performed twice weekly using 1% polidocanol as the sclerosing agent until the varices were eradicated or well-covered by fibrous tissue. Propranolol was given twice daily at a dose reducing the resting heart rate by 25% (60 to 320 mg per day; mean +/- SD = 161 +/- 80 mg per day). Patients were followed for up to 2 years with visits at 3 monthly intervals (mean follow-up = sclerotherapy, 14 months; propranolol, 9.2 months). Life table analysis of patients without rebleeding from nonvariceal sites revealed a tendency in favor of propranolol; however, the difference did not reach statistical significance. No significant difference was observed between sclerotherapy and propranolol in the proportion of patients rebleeding from esophageal varices or from all sources of upper gastrointestinal bleeding. Furthermore, survival was similar in both treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Combination of ketanserin and verapamil or propranolol in patients with alcoholic cirrhosis: search for an additive effect.

Drugs reported to reduce portal pressure through different mechanisms were combined in the hope of either additive portal hypotensive effects in "responders," or inducing a portal hypotensive effect in "nonresponders" to the initial drug. Seven patients with alcoholic cirrhosis received verapamil, 10 mg i.v., and, 60 min later, ketanserin, 5 mg i.v. Verapamil decreased heart rate and increased free hepatic venous pressure but had no effect on hepatic venous pressure gradient or azygos blood flow. When combined with verapamil, ketanserin significantly diminished wedged hepatic venous pressure and hepatic venous pressure gradient. Ten other patients with alcoholic cirrhosis received propranolol, 15 mg i.v., and 45 min later, ketanserin, 5 mg i.v. In all patients, heart rate, cardiac index and azygos blood flow significantly decreased after propranolol. After propranolol alone, however, wedged hepatic venous pressure decreased in only five patients, responders. In five other patients, defined as nonresponders, propranolol did not decrease this pressure. The addition of ketanserin to propranolol induced further significant reduction in wedged hepatic venous pressure, hepatic venous pressure gradient and azygos blood flow. Among the five nonresponders, three had a reduced wedged hepatic venous pressure after ketanserin was combined. We conclude that verapamil does not reduce portal pressure or collateral blood flow in patients with alcoholic cirrhosis. The splanchnic hemodynamic effects of propranolol and ketanserin appear to be independent and additive, without significant systemic alteration.

Drug Synergism↗
PubMed1990

Rabbit hepatocytes in primary culture: preparation, viability and use in studies of propranolol metabolism.

Isolated hepatocyte cultures have become a frequently used model system for investigating drug metabolism. Although rat and hamster hepatocytes are frequently used for this purpose, metabolism in these species differs in many respects from human metabolism. A species with a metabolism more closely resembling that of humans might be more useful. Our in vivo experiments demonstrated that the metabolism of propranolol in the rabbit is more similar to that in humans than in rats or hamsters. We therefore examined the usefulness of rabbit parenchymal liver cells for studies of propranolol metabolism. A detailed method is presented for their preparation and culture, along with data on their viability, structure and protein synthesizing capability. One- or two-day-old hepatocyte cultures were exposed to 10 mumol/L 3H-propranolol from 30 min to 2 hr; metabolites were identified by gas chromatography-mass spectrometry and quantitated by high-performance liquid chromatography. Propranolol metabolism was linear over 1 hr, with 15% of the substrate metabolized during this time. The cytochrome P-450 pathways, which result in ring oxidation and side-chain oxidation, were expressed in a reproducible fashion similar to that found in vivo in humans. The arylhydrocarbon hydroxylase inhibitor alpha-naphthoflavone (100 mumol/L) inhibited side-chain oxidation of propranolol by 90% without affecting ring oxidation. In contrast, chlorpromazine (100 mumol/L) was shown to inhibit ring oxidation of propranolol by 85% without affecting side-chain oxidation. Cimetidine (250 mumol/L) inhibited both pathways by about 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Combined treatment of portal hypertension with ritanserin and propranolol in conscious and unrestrained cirrhotic rats.

We recently reported that ritanserin, a 5-hydroxytryptamine receptor antagonist, induced significant reduction of portal pressure in cirrhotic rats. In this study, we investigated the hemodynamic effects of a combination of propranolol and ritanserin in conscious and unrestrained cirrhotic rats. Heparinized catheters exiting from the neck were placed into the portal vein, inferior vena cava, aorta and left ventricle. Cardiac output and regional blood flows were measured with radiolabeled microspheres and the reference-sample method. Serial hemodynamic studies were performed 4 hr after rats awakened (basal), 1 hr after administration of ritanserin (0.63 mg/kg body wt, intravenously) and after intravenous propranolol infusion (0.33 mg/kg/min for 15 min) in nine cirrhotic rats. Similar measurements were obtained in a control group of eight cirrhotic rats treated with the solvents of ritanserin and propranolol. Ritanserin caused significant reduction of portal pressure (-19%). Portal-venous inflow and splanchnic arteriolar resistances remained unchanged, whereas portal-venous resistances were slightly but significantly lowered (-17%); and ritanserin had no effects on systemic hemodynamics. The addition of propranolol resulted in further reduction of portal pressure (-24%); the final reduction after combined therapy was -38%. Propranolol induced a marked decrease in cardiac output (-31%) and portal-venous inflow (-30%). It also caused a significant increase in splanchnic arteriolar resistance (+39%), but did not magnify the ritanserin-induced decrease of portal-venous resistance. The combined therapy did not modify the mean arterial pressure. Our results show that the effects of ritanserin on portal pressure--probably mediated by a reduction of intrahepatic and/or portocollateral resistances--can be potentiated by propranolol, which lowers the portal-venous inflow.

Animals↗
PubMed1993

Effects of propranolol on gastric mucosal perfusion in cirrhotic patients with portal hypertensive gastropathy.

This study investigated the effects of the short-term administration of propranolol on gastric blood perfusion in cirrhotic patients with portal hypertensive gastropathy. Portal hypertensive gastropathy is a common cause of nonvariceal bleeding in cirrhosis, which is associated with increased gastric mucosal perfusion and is favorably influenced by propranolol therapy. Gastric mucosal perfusion was evaluated with laser-Doppler flowmetry and reflectance spectrophotometry. Measurements were performed under basal conditions and after the double-blind administration of propranolol (0.15 mg/kg intravenously) or placebo. Propranolol administration significantly reduced (p < 0.001) the laser-Doppler signal (2.93 +/- 0.23 vs. 2.25 +/- 0.22 V) and the hemoglobin content of the gastric mucosa (99.2 +/- 3.8 vs. 89.3 +/- 3.1 arbitrary units), whereas the oxygen content remained unchanged (37.4 +/- 1.2 vs. 36.9 +/- 1.0 arbitrary units). Placebo administration had no effect in any of these parameters. Changes in gastric perfusion after propranolol administration were associated with a significant decrease in hepatic venous pressure gradient and azygos blood flow. We conclude that short-term propranolol administration, in addition to lowering portal pressure, reduces the increased gastric blood perfusion in cirrhotic patients with portal hypertensive gastropathy, an effect that may contribute to prevention of bleeding from these lesions.

Female↗
PubMed2006

Influence of beta-2 adrenergic receptor gene polymorphism on the hemodynamic response to propranolol in patients with cirrhosis.

The beta-2-adrenergic receptor (beta(2-)-AR) has several single-nucleotide polymorphisms. These influence the functional response to adrenergic stimulation; genotypes homozygous for Gly16-Glu27 or Gly16-Gln27 alleles (Gly16-Glu/Gln27 haplotypes) are associated with enhanced response, whereas genotypes homozygous for Arg16-Gln27 alleles (Arg16-Gln27) show a decreased response. We hypothesized that gene polymorphisms at the beta2-AR may influence the hemodynamic response to propranolol in patients with cirrhosis. The beta2-AR gene polymorphisms were determined by direct sequencing of the polymerase chain reaction (PCR) products in 48 patients with cirrhosis. All patients also had hepatic and systemic hemodynamic studies before and after propranolol administration. Prevalence of Gly16-Glu/Gln27 haplotypes was 29.1%, Arg16-Gln27 haplotype was 16.7%, and 54.2% were compound heterozygotes. Patients with cirrhosis with Gly16-Glu/Gln27 haplotypes had a greater decrease in heart rate, cardiac index, and hepatic blood flow after propranolol administration than those with Arg16-Gln27 haplotype. However, the HVPG response to propranolol was similar in both groups, whereas estimated hepatic sinusoidal resistance increased significantly in Gly16-Glu/Gln27 haplotypes but not in Arg16-Gln27 (+27.1 +/- 17.8% vs -17.9 +/- 13.9%, P = .042), suggesting that unopposed vasoconstrictive activity at the intrahepatic circulation hinders the fall in HVPG despite enhanced hemodynamic response to propranolol in Gly16-Glu/Gln27 haplotypes. In conclusion, beta2-AR gene polymorphisms influence the response to beta-blockade. However, HVPG reduction cannot be predicted from polymorphism analysis. Patients with the Gly16-Glu/Gln27 haplotypes may benefit from the association of hepatic vasodilators to propranolol therapy.

Adult↗
PubMed1998

Effects of propranolol on the hepatic hemodynamic response to physical exercise in patients with cirrhosis.

Physical exercise increases portal pressure (hepatic venous pressure gradient [HVPG]) in patients with cirrhosis. It is unknown if this deleterious effect is associated with changes in gastroesophageal collateral blood flow and if these can be prevented by propranolol administration. The aim of this study was to characterize the effects of propranolol on the splanchnic hemodynamic response to exercise in patients with cirrhosis. Twenty-three patients with cirrhosis and portal hypertension had hemodynamic measurements in baseline conditions, and during moderate cycling exercise (40 W) under double-blind propranolol or placebo administration. In patients receiving placebo, HVPG significantly increased during exercise (from 16.7 +/- 0.9 to 19.0 +/- 1.0 mm Hg; P < .01), hepatic blood flow (HBF) decreased (-18% +/- 4%; P < .01), while azygos blood flow (AzBF) was unchanged (4% +/- 12%; ns). In patients receiving propranolol, portal pressure did not increase during exercise, but decreased from 16.3 +/- 1.0 to 12.9 +/- 1.1 mm Hg (P < .01). The lack of increase in HVPG in response to exercise in patients receiving propranolol may be related to a more pronounced decrease in HBF, as compared with patients receiving placebo, and to a blunted increase in cardiac output (CO). Moderate physical exercise adversely influences the hepatic hemodynamics in patients with cirrhosis, causing a significant increase in portal pressure. This is effectively prevented by propranolol pretreatment.

Adrenergic beta-Antagonists↗