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PubMed1992

Age-related delay in recovery of beta-adrenergic sensitivity after abrupt propranolol withdrawal in rats.

We compared cardiovascular responses to various adrenergic agonists in conscious 3-month and 12-month old rats that had been treated with propranolol daily for 7 days, to determine whether changes in beta-adrenergic hypersensitivity induced by abrupt propranolol withdrawal would differ with age. Depressor and tachycardic responses elicited by beta-adrenergic stimulation with isoproterenol were still reduced during the first 3 days following propranolol withdrawal, but were restored to pretreatment levels, more slowly in 12-month than in 3-month-old rats. Opposite pressor and bradycardic responses to alpha-adrenergic stimulation with phenylephrine did not differ between age groups, either before or after propranolol withdrawal. By contrast, pressor and bradycardic responses produced by combined alpha- and beta-adrenergic stimulation with epinephrine after propranolol withdrawal, though unaltered in 3-month-old rats, were enhanced in 12-month-old rats. Hence after sudden propranolol withdrawal beta-adrenergic sensitivity in conscious rats was gradually restored, rather than being enhanced, but more slowly at 12 than at 3 months of age. These results suggest that following abrupt cessation of prolonged propranolol treatment, restoration of normal beta-adrenergic sensitivity becomes delayed in older rats.

Aging↗
PubMed1983

Synergistic effect of propranolol and quipazine on desipramine enhanced shock-elicited fighting in rats.

Changes in shock-elicited fighting (SEF) were measured following single or repeated injections (IP) of dl-propranolol (5 mg/kg, 20 mg/kg) or quipazine (1.25 mg/kg, 2.5 mg/kg) given either alone or in combination to saline or desipramine (DMI) (10 mg/kg) treated rats. DMI + propranolol (20 mg/kg) caused a greater increase in fighting than DMI + saline 18 hours after last dose. Propranolol (20 mg/kg) produced an equal inhibition in both of these groups at 15 min. Propranolol (5 mg/kg) had no effect. Quipazine (2.5 mg/kg) failed to alter DMI induced increase in SEF. The combination of propranolol (5 mg/kg) + quipazine (1.25 mg/kg) blocked the enhanced SEF significantly in DMI treated rats in comparison to DMI + saline treated group. This combination of propranolol + quipazine produced no significant change in SEF in saline treated group in comparison to the pretest level. These results suggested that propranolol + quipazine act synergistically at low doses to inhibit the increased SEF seen in DMI treated rats and might have therapeutic implications for the management of irritable aggression or mania.

Aggression↗
PubMed1987

A new method of inhalation challenge with propranolol: comparison with methacholine-induced bronchoconstriction and role of vagal nerve activity.

To establish a safe procedure for examining propranolol-induced bronchoconstriction, we have developed a new method for performing inhalation challenge with propranolol. Monitoring respiratory resistance during tidal breathing with continuous inhalation of propranolol in 1.5-fold increasing concentrations from 0.78 to 30 mg/ml for 1 minute at each concentration, we tested 43 subjects with stable asthma and 10 normal subjects. We also compared bronchial responsiveness with responsiveness to inhaled methacholine on separate days. In addition, to determine the role of vagal nerve activity in propranolol-induced bronchoconstriction, we studied the effect of atropine. Inhaled propranolol caused dose-related bronchoconstriction in all subjects with asthma but not in normal subjects. None of the subjects suffered severe asthmatic attack during the test, which was performed in 15 minutes or less. The minimum cumulative dose of methacholine and of propranolol, at the point where respiratory conductance began to decrease, was not significantly correlated. Increased respiratory resistance was reversed by atropine in 70% of the subjects with asthma with marked individual differences. These data suggest that, although in most subjects with asthma, vagal nerve activity contributes in varying degree to bronchoconstriction, other constricting factors may contribute in the remaining subjects. It is also suggested that the mechanism of bronchial response to propranolol differs from that of the nonspecific airway reactivity estimated by methacholine challenge.

Adolescent↗
PubMed1991

Propranolol in prevention of recurrent bleeding from severe portal hypertensive gastropathy in cirrhosis.

The two main causes of gastrointestinal bleeding in cirrhosis are oesophageal varices and portal hypertensive gastropathy (PHG). Rebleeding from varices can be prevented by beta-blockers, but it is not clear whether these drugs effectively reduce rebleeding from PHG. 54 cirrhotic patients with acute or chronic bleeding from severe PHG took part in a randomised, controlled trial to investigate the efficacy of propranolol in prevention of rebleeding from PHG. 26 patients were randomised to receive propranolol daily at a dose that reduced the resting heart rate by 25% or to 55 bpm (20-160 mg twice daily), throughout mean follow-up of 21 (SD 11) months. 28 untreated controls were followed-up, with the same examinations, for 18 (13) months. The actuarial percentages of patients free of rebleeding from PHG were significantly higher in the propranolol-treated patients than in the untreated controls at 12 months (65% vs 38%; p less than 0.05) and at 30 months of follow-up (52% vs 7%; p less than 0.05). Propranolol-treated patients had fewer episodes of acute bleeding than controls (0.010 [0.004] vs 0.120 [0.040] per patient per month). Multivariate analysis showed that absence of propranolol treatment was the only predictive variable for rebleeding. Actuarial survival was slightly higher in the propranolol group than in the controls, but the difference was not significant. Thus, long-term propranolol treatment significantly reduces the frequency of rebleeding from severe PHG, and may improve the prognosis of cirrhotic patients with this disorder.

Actuarial Analysis↗
PubMed1990

The membrane stabilizing and beta 1-adrenoceptor blocking activity of (+)- and (-)-propranolol on the rat left atria.

1. The membrane stabilizing and beta 1-adrenoceptor blocking activities of (+)- and (-)-propranolol have been determined using the rat left atria. 2. (+)- And (-)-propranolol have membrane stabilizing activity. Thus a low concentration of (-)-propranolol, 10(-8) M, and a higher concentration of (+)-propranolol, 10(-6) M, inhibited the responses to electrical stimulation. A high concentration of (+)- and (-)-propranolol, 10(-5) M, also inhibited the maximal combined response to electrical stimulation and isoprenaline. 3. As competitive beta 1-adrenoceptor antagonists, (-)-propranolol was over a 100 times more potent than (+)-propranolol.

Adrenergic beta-Antagonists↗
PubMed1993

Pharmacologic modulation of the autonomic nervous system in the prevention of sudden cardiac death. A study with propranolol, methacholine and oxotremorine in conscious dogs with a healed myocardial infarction.

OBJECTIVES: The goal of the present study was to evaluate the antifibrillatory and hemodynamic effects of pharmacologic muscarinic activation and to compare them with those of beta-adrenergic blockade. BACKGROUND: Recent studies suggest a correlation between increased vagal activity and a reduced incidence of sudden cardiac death. Electrical stimulation of the vagus nerve reduces the incidence of ventricular fibrillation in a conscious animal model of sudden cardiac death. METHODS: Eleven dogs with healed anterior myocardial infarction, in which a 2-min left circumflex coronary artery occlusion during exercise caused ventricular fibrillation, were studied. They underwent subsequent tests with saline solution, propranolol (1 mg/kg body weight), methacholine (0.5 microgram/kg per min) and oxotremorine (8 micrograms/kg). RESULTS: In the test with saline solution, 100% of the dogs developed ventricular fibrillation; this occurred in only 10% of the tests with propranolol (95% confidence interval 0.2% to 44%; p < 0.001), 60% of the tests with methacholine (95% confidence interval 26% to 88%, p = 0.05) and 37.5% of the tests with oxotremorine (95% confidence interval 8% to 75%, p = 0.005). Propranolol and oxotremorine significantly reduced heart rate compared with saline solution, whereas methacholine did not. Propranolol significantly reduced maximal first derivative of left ventricular pressure, (dP/dtmax), particularly during myocardial ischemia, compared with the other treatments (2,391 +/- 582 mm Hg/s [mean +/- 1 SD] with propranolol vs. 4,226 +/- 1,237, 4,922 +/- 584 and 4,358 +/- 1,109 mm Hg/s with saline solution, methacholine and oxotremorine, respectively, p < 0.005). CONCLUSIONS: Propranolol was extremely effective against ventricular fibrillation. Methacholine and oxotremorine provided a significant, although less marked, protection and caused much less impairment of contractility compared with propranolol. Muscarinic receptor activation may represent a new approach to prevention of sudden cardiac death, particularly when beta-blockers are contraindicated and negative inotropic effects are to be avoided.

Animals↗
PubMed1994

Expansion of aortic aneurysms is reduced by propranolol in a hypertensive rat model.

PURPOSE: It has been suggested that propranolol has unique effects that slow aneurysm expansion by remodeling the structural proteins of the aorta. These effects are believed to be independent of blood pressure reduction, a hypothesis we tested in this investigation with a rat model of abdominal aortic aneurysm (AAA). METHODS: With an established model, AAA were induced in normotensive Wistar-Kyoto (WKY) rats and genetically hypertensive Wistar-Kyoto (WKHT) rats by perfusing an isolated segment of the infrarenal aorta with elastase. A propranolol dose-response was studied for each strain: (1) saline solution controls (n = 18); (2) propranolol, 10 mg/kg subcutaneously (n = 18); (3) propranolol, 30 mg/kg (n = 14). Systolic blood pressure was determined by tail plethysmography before operation and on day 14, as well as by direct recording at surgery and on day 14. Rats were killed at 14 days, and aneurysm diameter was measured. RESULTS: The initial tail BP was 129 +/- 22 mm Hg in WKY animals and 158 +/- 21 mm Hg in WKHT animals (p < 0.0001). Tail BP and intraaortic systolic, diastolic, and mean blood pressure (BP) were not significantly decreased by propranolol treatment in either strain of rats. However, BP tended to rise in WKY rats, whereas it fell slightly in WKHT rats. Initial aortic size in all animals was 1.06 +/- 0.12. The final aortic size in untreated, hypertensive rats was more than twice that of untreated normotensive controls: 1: WKHT, 3.0 +/- 0.73 mm, 1: WKY, 6.9 +/- 3.5 mm (p < 0.01). After treatment with both doses of propranolol, hypertensive aneurysms were significantly smaller than the untreated WKHT group (p < 0.05) and not significantly different from aneurysms in all groups of normotensive animals: 2: WKY, 3.1 +/- 1.13 mm, 2: WKHT, 4.0 +/- 1.81 mm; 3: WKY, 4.1 +/- 0.41 mm, 3: WKHT, 2.9 +/- 1.24 mm. There was no significant difference in aortic size between the three normotensive WKY groups. CONCLUSIONS: Hypertension increases the size of aortic aneurysms in this experimental model. Propranolol significantly reduces the size of experimental AAA in hypertensive animals independently of the dose and by a mechanism that may be unrelated to simple BP reduction.

Analysis of Variance↗
PubMed2006

Low-dose mirtazapine: a new option in the treatment of antipsychotic-induced akathisia. A randomized, double-blind, placebo- and propranolol-controlled trial.

BACKGROUND: Preliminary evidence indicates a beneficial effect of serotonin 2A (5-HT(2A)) receptor antagonists in antipsychotic-induced akathisia (AIA). We investigated the antiakathisia effect, safety, and tolerability of low-dose mirtazapine, an agent with marked 5-HT(2A) antagonism. METHODS: In a 7-day double-blind trial, 90 antipsychotic-treated patients meeting DSM-IV criteria for AIA were randomly assigned to mirtazapine (n = 30; 15 mg), propranolol (n = 30; 80 mg), or placebo (n = 30). Primary outcome measures were between-group differences in Barnes Akathisia Scale (BAS) global scores and in the proportion of responders (reduction of > or = 2 points on BAS). Analysis was by intention to treat. RESULTS: Twenty-four patients (26.6%) who were assigned treatment did not complete the study (7 mirtazapine, 8 propranolol, 9 placebo), due to lack of response (n = 19) and adverse events (n = 5). Both mirtazapine and propranolol significantly reduced AIA severity (BAS: -34% mirtazapine and -29% propranolol vs. placebo -11%; p = .012 and p = .023, respectively). Thirteen (43.3%) mirtazapine and 9 (30.0%) propranolol-treated patients versus 2 (6.7%) placebo-treated patients responded (the corresponding odds ratios 10.7 [95% confidence interval (CI), 2.1-53.3] and 6.0 [95% CI, 1.1-30.7]). Five (16.7%) of 30 propranolol-treated patients and none in the mirtazapine and placebo groups (p = .0195 for both) prematurely discontinued the study due to clinically significant hypotension or bradycardia. CONCLUSIONS: The comparable efficacy and better tolerability of low-dose mirtazapine versus propranolol, the current first-line treatment for AIA, position mirtazapine as a favorable candidate for the treatment of acute AIA and may improve current therapeutic practices.

Adult↗
PubMed2006

Pravastatin reverses the down-regulating effect of inflammation on beta-adrenergic receptors: a disease-drug interaction between inflammation, pravastatin, and propranolol.

Inflammatory conditions reduce the potency to prolong the PR interval of certain cardiovascular drugs including propranolol, sotalol, and verapamil in rats and humans despite elevated plasma drug concentrations. We tested whether pravastatin restores altered action and disposition of propranolol as well as inflammatory mediators concentrations in the Pre-Adjuvant Arthritis (Pre-AA) Sprague-Dawley rat model. Rats [Healthy/Placebo, Arthritis/Placebo, Healthy/Statin, and Arthritis/Statin groups (n=14-16/group)] received Mycobacterium butyricum on day 0 followed by 6 mg/kg pravastatin or placebo twice daily during days 4-8. PR-interval response to 25 mg/kg oral propranolol was measured on days 0, 4 and 8. On day 8, blood samples were collected for interferon-gamma, interleukin-10, C-reactive protein, and nitrite measurements. Propranolol enantiomer pharmacokinetics were delineated using another 4 groups (healthy n=5, Pre-AA n=9) on day 8. Pre-AA significantly reduced propranolol response despite a 10-fold increase in concentrations. Pravastatin restored the response but not the drug concentrations. Area under the % effect-time curve (% min) was 714+/-214 in Healthy/Placebo, 256+/-249 in Arthritis/Placebo, 1534+/-367 in Healthy/Statin, and 1713+/-393 in Arthritis/Statin. While pravastatin reduced elevated serum interferon-gamma concentration in the Pre-AA model, it did not influence other biomarkers. Pravastatin restores response to propranolol in inflamed rat but has no effect on the elevated propranolol concentrations. This was associated with lower serum interferon-gamma concentrations.

Adrenergic beta-Antagonists↗
PubMed1977

Propranolol for patients with mitral valve prolapse.

This study evaluates propranolol's effect on symptoms, arrhythmias, and exercise tolerance in 16 patients with mitral valve prolapse. Three patients (19 per cent) experienced symptomatic deterioration with propranolol therapy, seven (44 per cent) were unchanged, and six (37 per cent) noted an over-all symptomatic improvement, primarily due to a reduction in palpitation. Symptomatic improvement continues in these six patients an average of 12.5 months after beginning propranolol therapy. Treatment with propranolol alleviated chest pain in only two of eight patients and it did not improve the ability to perform treadmill exercise. Fatigue did not improve, and in three patients appeared for the first time during propranolol therapy. Premature ventricular contractions were reduced by at least 75 per cent in five of nin patients (56 per cent), and paroxysmal ventricular tachycardia was eliminated in three of four patients. We conclude that propranolol is not uniformly effective in patients with mitral vale prolapse. A trial of propranolol may be instituted fro patients with mitral valve prolapse who have severe symptoms and/or arrhythmias, but the drug should only be continued in those who demonstrate clinical and/or antiarrhythmic response.

Adult↗
PubMed1983

Biphasic nature of propranolol's microelectrophysiologic effects.

The microelectrophysiologic effects of d,l-propranolol were observed to be biphasic when a wide range of concentrations was used in canine atrial tissue; therefore, the 2 isomers were used separately to test the hypothesis that the opposite effects of propranolol could be separated by isomeric isolation. Whole atria were detached from dog hearts and 3 by 0.5 cm strips were cut from the atria. Transmembrane action potentials were monitored from the atrial strips mounted in an isolation chamber containing Tyrode's solution. Concentrations of d-propranolol, l-propranolol, and the d,l-racemate ranging from 0.03 to 1.0 micrograms/ml were added to the bath and the effects observed for 60 minutes. In lower concentrations d,l-propranolol decreased the effective refractory period and activation time while increasing maximal rise velocity, action potential amplitude, and resting membrane potential. Higher concentrations produced the opposite effects. The l-isomer produced effects very similar to those of the lower concentrations of the racemate, whereas the d-form mimicked those effects of the higher concentrations of the racemic mixture. We conclude that d,l-propranolol is capable of exerting 2 opposite electropharmacologic actions, which may be demonstrated by varying the concentration of d,l-propranolol or by separating the isomers.

Action Potentials↗
PubMed1989

Superior efficacy of propranolol versus nifedipine in double-component angina, as related to different influences on coronary vasomotility.

PURPOSE: In 24 patients with stable spontaneous and effort-related angina, ischemic episodes at rest were not preceded by changes in circulatory variables (heart rate, systemic and pulmonary arterial pressures) that may raise the myocardial oxygen consumption. We interpreted these episodes as caused by critical and reversible coronary flow reduction at the site of a stenotic lesion, and evaluated the clinical efficacy of nifedipine and propranolol in the treatment of this condition. PATIENTS AND METHODS: The study was randomized, placebo-controlled, and crossover in design. Nineteen of the 24 subjects were men (mean group age, 59 years; range, 47 to 65 years). The study consisted of four four-day periods. The first and the fourth periods, during which patients received placebo, were single-blind. The treatment consisted of 80 mg of propranolol or 20 mg of nifedipine administered four times daily. The second and the third periods, during which patients received propranolol or nifedipine crossing over to the alternative drug in the next period, were double-blind and separated by a 24-hour interval. RESULTS: Propranolol fully abolished or reduced the number of spontaneous ischemic episodes in a significantly larger proportion of patients than did nifedipine; it was also effective in several cases in which nifedipine had failed or had even caused a paradoxic effect. Quantitative angiographic evaluation of the influences of nifedipine (Group 1, 12 patients, 10 mg sublingually) and propranolol (Group 2, 12 patients, 0.1 mg/kg intravenously) on the residual lumen diameter of one significant coronary stenosis in each patient showed that (1) after nifedipine, the lumen was unchanged in one, augmented in seven, and reduced in four cases; (2) variations ranged between +1.59 and -1.2 mm, and their direction correlated closely with the influence of oral nifedipine on the episodes of spontaneous ischemia; and (3) in no case did treatment with propranolol vary the stenosis lumen by more than 0.3 mm. CONCLUSION: In this form of angina, a number of lesions seem to offer a compliant substrate for vasomotion and, possibly, for critical changes in flow. The vasomotor influences of nifedipine on these lesions are variable as well as the efficacy of the drug on the manifestations of ischemia at rest. Propranolol produces no important variations of the coronary stenotic lesions, causes a decrease of heart rate that facilitates coronary flow in diastole, and reduces the baseline metabolic demand of the heart so that the threshold of ischemia during critical reduction of coronary flow may become elevated.

Aged↗
PubMed2002

Total effective vascular compliance in patients with cirrhosis. Effects of propranolol.

BACKGROUND: Total effective vascular compliance (TEVC), may be increased in cirrhosis. However, its significance is unclear. AIMS: To investigate TEVC in patients with cirrhosis, and the effects of propranolol. METHODS: Seven patients without liver disease and 44 cirrhotic patients were studied before and after double-blind administration of propranolol (n=33) or placebo (n=11). MEASUREMENTS: TEVC (right atrial pressure response to rapid central volume expansion), hepatic venous pressure gradient (HVPG) and systemic hemodynamics. RESULTS: TEVC (ml x mmHg(-1) x kg(-1)) was increased in cirrhotics (1.67 +/- 0.66 versus 1.33 +/- 0.32 in controls; P<0.05). TEVC was not modified by placebo, but was markedly reduced by propranolol (from 1.74 +/- 0.75 to 1.33 +/- 0.56; P<0.01). Propranolol decreased HVPG >10% in 20 patients ('responders': -20 +/- 9%) but <10% in 13 'non-responders'. TEVC was normalized by propranolol in HVPG 'responders' (from 1.76 +/- 0.88 to 1.21 +/- 0.51; P<0.01), but not in 'non-responders' (1.69 +/- 0.48 to 1.52 +/- 0.59; NS). Reduction of TEVC in responders was accompanied by increased free hepatic vein pressure (+21 +/- 20%, P=0.05; approximately 60% of the fall in HVPG), which was not observed in non-responders (+3 +/- 11%, NS). CONCLUSIONS: TEVC is increased in cirrhosis. This abnormality is corrected by propranolol in patients exhibiting a >10% fall in HVPG, suggesting that changes in vascular compliance may influence the portal pressure response to propranolol.

Compliance↗
PubMed1993

Effects of terlipressin on hemodynamics and oxygen content in conscious portal vein stenosed and cirrhotic rats receiving propranolol.

Terlipressin is used in patients with variceal bleeding but its effects in patients receiving beta-adrenergic antagonists are unknown. In this study, the hemodynamic effects of terlipressin were evaluated in conscious portal hypertensive rats which had previously received a single dose of propranolol. Moreover, oxygen content and acid-base status were studied. In portal vein stenosed and cirrhotic rats, the addition of terlipressin (0.05 mg/kg) to propranolol (0.4 mg/kg) produced a decrease in portal pressure of 34% and 17%, respectively, and in portal tributary blood flow of 46% and 42%, respectively. In cirrhotic rats, however, the decrease in portal pressure was not significantly different when propranolol was combined with terlipressin than when propranolol was administered alone. Cardiac index also further decreased after terlipressin administration. In both groups of rats, these values were similar to those observed after terlipressin alone. In portal vein stenosed rats but not in cirrhotic rats, arterial pH was significantly lower following the combination of propranolol plus terlipressin than following saline, propranolol or terlipressin alone. In conclusion, terlipressin further reduces both portal pressure and cardiac index in rats with portal hypertension receiving beta-blockers. In portal vein stenosed rats but not in cirrhotic rats, the addition of terlipressin to propranolol induces acidemia. This study suggests that terlipressin might further reduce portal pressure in patients with portal hypertension treated with beta-blockers.

Animals↗
PubMed1985

Acute effect of propranolol on splanchnic circulation in normal and portal hypertensive rats.

Propranolol decreases portal venous pressure in patients with cirrhosis but no method is available in man to study the effect of this beta-blocker on splanchnic organ blood flow. Because in rats, the microsphere method allows evaluation of regional blood flow, the acute effect of propranolol on both splanchnic and systemic circulations was studied in normal rats and in rats with portal hypertension due to portal vein stenosis. Portal venous pressure significantly decreased during propranolol administration in normal (5.6 +/- 1.0-4.7 +/- 1.1 mm Hg; mean +/- SD) as well as in portal hypertensive rats (11.7 +/- 2.3-10.3 +/- 1.8 mm Hg). Propranolol slightly decreased cardiac output and arterial pressure in all rats. Portal tributary blood flow was significantly reduced by propranolol in normal rats (17.4 +/- 3.0-11.3 +/- 2.2 ml/min) and in portal hypertensive rats (23.7 +/- 5.0-16.6 +/- 3.3 ml/min). Accordingly vascular resistance of the different organs in the portal venous territory increased in these rats receiving propranolol. The percentage of the decrease in portal tributary blood flow was significantly more marked than the percentage of reduction in cardiac output in portal hypertensive rats but, in normal rats, these percentages were parallel. Hepatic arterial blood flow did not change or slightly increased and, consequently, hepatic arterial vascular resistance decreased. These findings further clarify the marked effects of propranolol on splanchnic circulation.

Animals↗
PubMed1987

Reversal of adrenaline-induced increase in azygos blood flow in patients with cirrhosis receiving propranolol.

In patients with cirrhosis, endogenous catecholamines may influence the circulatory effects of propranolol. We intended to evaluate the interaction of adrenaline and propranolol on azygos blood flow, an estimate of blood flow in the superior portosystemic collateral circulation. We investigated 6 patients with cirrhosis, 5 with good liver function, receiving an intravenous infusion of adrenaline (50 ng/kg/min) before and after administration of propranolol. The median value for baseline azygos blood flow was increased from 700 ml/min (range 340-1 470 ml/min) to 1 050 (range 570-1 840 ml/min) with adrenaline alone (P less than 0.05), and decreased to 610 ml/min (range 260-1 190 ml/min) with propranolol alone (P less than 0.05). The infusion of adrenaline given after propranolol further reduced azygos blood flow to a median value of 530 ml/min (range 200-730 ml/min) (P less than 0.05). Thus, following beta-adrenergic blockade, there is a reversal of the effects of adrenaline on azygos blood flow, which corresponds to a potentiation of the effects of propranolol. Similar endogenous adrenaline-propranolol interactions may play a role in preventing recurrent variceal bleeding in cirrhotic patients.

Adult↗
PubMed1988

Effect of propranolol on metabolic activity of the liver in patients with alcoholic cirrhosis.

Many studies have been performed to investigate the haemodynamic effects of propranolol. However, little is known of its actions on the metabolic activity of the liver. This study aimed to investigate the influence of propranolol on hepatic function as assessed by the galactose elimination capacity (GEC) and the intrinsic clearance of indocyanine green (ICG). 15 patients with biopsy-proven alcoholic cirrhosis and portal hypertension were studied. 10 had GEC and ICG clearance measured before and after the i.v. injection of 15 mg of propranolol (group P) and 5 had ICG clearance measurement before and after normal saline injection (group C). Propranolol significantly reduced heart rate (P less than 0.005) and the porto-hepatic pressure gradient (P less than 0.01). Hepatic blood flow was not changed. GEC was not altered by propranolol. Propranolol decreased the intrinsic hepatic clearance of ICG as determined by the 'sinusoidal' model by 12% (P less than 0.01). This suggests that propranolol may have an inhibitory action on the hepatic elimination of ICG that is independent of any effect on total liver blood flow or drug metabolism, since intrinsic clearance is not influenced by changes in blood flow and ICG is thought not to be metabolized.

Female↗
PubMed1980

Simultaneous determination of d- and l-propranolol in human plasma by high-performance liquid chromatography.

A method for the determination of d- and l-propranolol in human plasma is described. The method involves extraction of propranolol from plasma, and the formation of diastereomeric derivatives with the chiral reagent N-trifluoroacetyl-1-prolylchloride. Separation and quantitation of the diastereomeric propranolol derivatives are carried out by a reversed-phase high-performance liquid-chromatographic system with fluorimetric detection. The reproducibility in the determination of d- and l-propranolol in human plasma was 4.5% (relative standard deviation) at drug levels of 10 ng/ml. In two subjects who received a single 40-mg tablet of racemic propranolol the plasma levels of the d-isomer were lower than of the l-propranolol. The half-lives of d- and l-propranolol were similar.

Adult↗