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PubMed1979

Biochemical and haematological changes induced by tienilic acid combined with propranolol in essential hypertension.

Sixteen patients with moderate essential hypertension completed a double-blind crossover trial with four treatment periods each of 6 weeks. They received in random order: placebo; tienilic acid 250 mg/day; propranolol 80 mg twice daily; and tienilic acid 250 mg/day combined with propranolol 80 mg twice daily. Average blood-pressure in the lying position was 22.6/13.1 kPa (169/98 mm Hg) on placebo; 21.0/12.5 (157/94) on tienilic aicd; 21.2/12.0 (159/90) on propranolol, and 18.9/11.5 (142/86) on tienilic acid combined with propranolol. The effects of tienilic acid and propranolol on blood-pressure were additive and there were no statistically significant interactions. Tienilic acid significantly reduced serum-urate from 0.33 to 0.18 mmol/l and induced hypokalaemia which was corrected by propranolol. Basophil count and haemoglobin were lower after tienilic acid treatment than they had been at the start of the study.

Adult↗
PubMed2002

Chiral reversed phase high-performance liquid chromatography for determining propranolol enantiomers in transgenic Chinese hamster CHL cell lines expressing human cytochrome P450.

An enantioselective assay for S-(-)- and R-(+)-propranolol in transgenic Chinese hamster CHL cell lines, expressing human cytochrome P450 (CYP), was developed. The method involves extraction of propranolol from the S(9) incubates, using S-(+)-propafenone as internal standard, chiral derivatization with 2,3,4,6-tetra-O-beta-D-glucopranosyl isothiocyanate and quantitation by reversed phase high-performance liquid chromatography system with UV detection (lambda=220 nm). A baseline separation of propranolol enantiomers was achieved on a 5-microm reverse-phase ODS column, with a mixture of methanol/water/glacial acetic acid (67:33:0.05, v/v) as mobile phase. The assay is linear from 5 to 500 microM for each enantiomer. The analytical method affords average recoveries of 99.2% and 98.8% for S-(-)- and R-(+)-propranolol, respectively. The limit of quantitation for the method is 5 microM for both S-(-)- and R-(+)-propranolol. The reproducibility of the assay is satisfactory (RSD < 10%). The method allowed study of the depletion of S-(-)- and R-(+)-propranolol in transgenic Chinese hamster CHL cell lines expressing CYP3A4, CYP2C18 and CYP2C9.

Animals↗
PubMed1998

Effects of indirect light and propranolol on melatonin levels in normal human subjects.

An indirect lighting protocol was developed to measure nocturnal melatonin suppression by light in normal human subjects. Goals were to minimize both discomfort due to staring intensely at a bright light source, and behavioral variation due to wandering gaze. Subjects sat with a bank of five full-spectrum light sources placed behind them. Lights reflecting off the surfaces before each subject produced a hemisphere of light that measured 500 lx +/- 5%. Subjects retired to bed in darkness by midnight and then sat in the hemisphere of light from 02.00 h to 04.00 h. Blood for melatonin was drawn at 20-30-min intervals from midnight to 06.00 h. Plasma melatonin was measured by radioimmunoassay. The indirect lighting protocol was used to compare the effects of 500 lx light to dark (21 subjects) and to study varying light intensities from 300 to 2000 lx (7 subjects). We studied the effects of the sitting posture in very dim light of 20-30 lx (6 subjects). We also studied the effects of propranolol plus dark and propranolol plus 500 lx light on melatonin levels. Subjects received placebo, 10 mg propranolol or 40 mg propranolol orally at 23.00 h, and were then exposed to either the dark or light condition. Melatonin levels obtained with the indirect lighting protocol were consistent with studies using direct lighting; light of 500 lx significantly suppressed nocturnal melatonin and suppression was dose related between 300 and 2000 lx. Sitting in dim light had no significant effect on melatonin suppression when compared with the supine posture in the dark in six subjects. Propranolol caused a dose-dependent decrease in melatonin levels in both the dark and the light. There was no relationship between suppression of melatonin by propranolol and suppression by light.

Adolescent↗
PubMed1988

Hyperglucagonism and glucagon resistance in cirrhosis. Paradoxical effect of propranolol on plasma glucagon levels.

Propranolol, a non-selective beta-blocker, is known to decrease glucagon release in normal subjects. The present study was aimed at investigating the effects of propranolol on the hyperglucagonism commonly observed in patients with cirrhosis. Eight cirrhotic patients and 6 matched healthy controls were studied. The plasma concentrations of glucagon, insulin, c-peptide and glucose were measured in basal conditions and after stimulating glucagon secretion by an i.v. infusion of arginine (0.4 g/kg/30 min). The study was repeated 24 h later after inducing beta-blockade by the i.v. infusion of propranolol (10 mg). In baseline conditions, patients with cirrhosis, despite normal levels of insulin and glucose, had a marked hyperglucagonism (654 +/- 303 pg/ml vs. 269 +/- 90 in controls, P less than 0.01). Prior to propranolol, arginine infusion caused greater glucagon release in cirrhotics (71 +/- 31 ng.h.ml-1) than in controls (33 +/- 17 ng.h.ml-1, P less than 0.02), but despite a similar insulin secretion (assessed from c-peptide), blood glucose did not increase. After propranolol, glucagon secretion decreased as expected in controls (29 +/- 12 ng.h.ml-1, P less than 0.05) but experienced a paradoxical increase in cirrhotics (113 +/- 64 ng.h.ml-1, P less than 0.05). Again, despite the marked increase in glucagon release, there was no increase in glucose production, providing further evidence of the glucagon resistance that accompanies hyperglucagonism in cirrhosis. Our results suggest that hyperglucagonism with glucagon resistance might be the initial disturbance in carbohydrate metabolism in patients with cirrhosis. Contrary to what could be expected, propranolol does not correct but further accentuates this disturbance.

Adult↗
PubMed1988

Propranolol or endoscopic sclerotherapy in the prevention of recurrence of variceal bleeding. A prospective, randomized controlled trial.

Endoscopic sclerotherapy (ES) and continuous propranolol (P) treatment have both been proposed as useful methods to prevent recurrent esophageal variceal bleeding. We report a prospective randomized trial in 65 patients with a previous history of endoscopically proven esophageal variceal bleeding. Patients were randomized by sealed envelopes stratified for Child's A and B groups to receive either endoscopic sclerotherapy (n = 31) or propranolol (n = 34). The dose of oral propranolol was based on a reduction of the resting pulse rate by 25%. Intravascular ethanolamine oleate was used for the endoscopic sclerotherapy in a 3-week schedule. The follow-up period ranged from 17 to 57 months (median: ES = 31; P = 28 months). There was no difference in the cumulative percentages of patients free of rebleeding from any source: esophageal and gastric varices, acute esophageal and gastric ulcers or erosions (ES = 37%; P = 16%). Also, there was no difference in the cumulative survival (ES = 69%; P = 54%). However, patients in the propranolol group had significantly more variceal rebleeding from the esophagus (n = 21) than did those in the sclerotherapy group (n = 9). The cumulative percentages of patients free of esophageal variceal rebleeding after inclusion were 67% in the endoscopic sclerotherapy group and 25% in the propranolol group (log-rank test, P less than 0.02). These differences indicated that sclerotherapy should be used in 29% of the propranolol patients who rebled. Based on these results we recommend elective sclerotherapy as long-term therapy for preventing rebleeding of esophageal varices.

Adult↗
PubMed1997

Propranolol and sclerotherapy in the prevention of gastrointestinal rebleeding in patients with cirrhosis: a meta-analysis.

BACKGROUND/AIMS: A meta-analysis of nine selected randomized trials was performed to compare the effects of propranolol and sclerotherapy in the prevention of rebleeding and on survival in patients with cirrhosis. METHODS: Five end points were assessed: rebleeding, esophageal rebleeding, death, death due to bleeding, and adverse events. Analyses were performed according to the intention-to-treat method. For each end point, heterogeneity and treatment efficacy were assessed by the Der Simonian and Peto methods. When a significant difference was observed, sensitivity analyses were performed by successive stratification according to treatment duration, type of publication, severity of cirrhosis, and methodological quality. RESULTS: The mean percentage of patients free of rebleeding, the mean survival rate and the mean percentage of patients free of death from bleeding were not significantly different between patients treated with propranolol and those treated by sclerotherapy. The mean percentage of patients free of variceal rebleeding was 39% in propranolol group and 55% in sclerotherapy group (mean difference: 17%, 95% confidence interval: 9-25%, p < 0.001). The mean percentage of patients free of adverse events was significantly higher in the propranolol group than in the sclerotherapy group (mean difference: 22%, 95% confidence interval: 6-38%, p < 0.007). CONCLUSION: In patients with cirrhosis and esophageal varices, endoscopic sclerotherapy is more effective than propranolol in preventing variceal rebleeding, but the incidence of adverse events is significantly higher with sclerotherapy. There was no difference in survival between the treatments. Propranolol should be considered as a first choice treatment for preventing rebleeding.

Adult↗
PubMed1998

Noninvasive hemodynamic measurements of superior mesenteric artery in the prediction of portal pressure response to propranolol.

BACKGROUND/AIMS: The portal pressure response to propranolol administration is heterogeneous in patients with cirrhosis. The aim of this study was to examine the diagnostic accuracy of noninvasive hemodynamic parameters of superior mesenteric artery (SMA) and femoral artery (FA) in the prediction of portal pressure response to propranolol. METHODS: Twenty-six patients with cirrhosis were studied. Portal pressure was assessed by measurements of hepatic venous pressure gradient. Mean arterial pressure and heart rate were also recorded. Cardiac index, and flow velocity of SMA and FA, and pulsatility index of SMA and FA were then measured by means of Doppler ultrasonography. After intravenous propranolol administration (0.10 mg/kg), the above measurements were repeated. RESULTS: Propranolol significantly reduced cardiac index, heart rate, SMA flow velocity, and FA flow velocity and increased SMA pulsatility index and FA pulsatility index. Although propranolol significantly decreased hepatic venous pressure gradient, a reduction of > or =20% was seen in only 10 patients (good responders); the remaining 16 patients exhibited <20% reduction (poor responders). No significant differences in clinical and baseline hemodynamic data were found in the two groups. There were no also significant differences in changes in heart rate and cardiac index. However, reductions in SMA and FA flow velocity were significantly greater in good responders than in poor responders. Although there was no the increase in FA pulsatility index, the increase in SMA pulsatility index was significantly greater in good responders than in poor responders. When appropriate cut-off points were determined for these variables, overall predictive values of SMA flow velocity (-20%) and SMA pulsatility index (+15%) were 91% and 83%, whereas the overall predictive value of FA flow velocity (-25%) was only 69%. CONCLUSIONS: These results suggest that SMA flow velocity and SMA pulsatility index, but not FA flow velocity and FA pulsatility index, are useful noninvasive parameters in the prediction of portal pressure response to propranolol administration.

Adult↗
PubMed1996

Hemodynamic effects of calcium chloride in a canine model of acute propranolol intoxication.

STUDY OBJECTIVE: To evaluate the hemodynamic effects of calcium chloride in a canine model of acute propranolol toxicity. METHODS: Two minutes after the completion of a propranolol infusion (10 mg/kg), a bolus of .125 mL/kg 10% CaCl solution followed by an infusion of .375 mL/kg over the next 30 minutes or a bolus and subsequent infusion of an equivalent volume of normal saline solution was administered to each dog. RESULTS: CaCl yielded significant improvements in propranolol-induced decreases in cardiac index and stroke volume compared with saline solution-treated control animals (overall alpha = .05). Furthermore, CaCl administration resulted in earlier improvement in propranolol-induced alterations in mean arterial pressure, maximal left ventricular pressure change over time, and peripheral vascular resistance compared with saline solution (overall alpha = .05). We observed no difference between treatment groups in response to propranolol-induced bradycardia or QRS-interval prolongation. CONCLUSION: In this model of acute propranolol toxicity, CaCl therapy improved depressed hemodynamic status, mainly by a positive inotropic action.

Acute Disease↗
PubMed2000

Effect of propranolol and granisetron on experimentally induced pain and allodynia/hyperalgesia by intramuscular injection of serotonin into the human masseter muscle.

We have previously reported that intramuscular injection of serotonin (5-HT) into the masseter muscle elicits pain and allodynia/hyperalgesia in healthy subjects. The aim of this study was to investigate whether the 5-HT(3) receptor antagonist granisetron or 5-HT(1A) receptor antagonist propranolol can reduce 5-HT induced pain and allodynia/hyperalgesia in the masseter muscle. Twenty-four healthy individuals (12 males and 12 females) without pain from the masseter muscle region participated. They were examined clinically including tenderness to digital palpation (TDP) and pressure pain threshold (PPT) of the masseter muscle. 5-HT in combination with granisetron or propranolol was randomly injected on one side in a double-blind manner. 5-HT in combination with saline was used on the contralateral side. After the injections the pain intensity and PPT were recorded 10 times during 30min. After the last recording the TDP was assessed again. The injections were repeated with the other antagonist within 1 week. All three combinations of substances elicited pain after injection, which lasted for 5-8min. 5-HT induced significantly more pain than granisetron+5-HT and propranolol+5-HT. The TDP increased significantly after injection of all combinations of substances, but there was no significant difference between them. The PPT decreased significantly after injection of 5-HT and increased significantly after injection of granisetron+5-HT, while it did not change significantly after injection of propranolol+5-HT. The difference between 5-HT and granisetron+5-HT was significant. In conclusion, the results of this study indicate that injection of granisetron and propranolol into the human masseter muscle reduces pain induced by local administration of 5-HT, but that the effect of granisetron is stronger than that of propranolol. In addition, granisetron totally abolishes allodynia/hyperalgesia.

Adult↗
PubMed1997

Influence of hypothermia on the cardiac effects of propranolol observed in isolated rat atria.

UNLABELLED: 1. The purpose was to determine if hypothermia influences cardiac responses to propranolol. 2. Rat atria were used and 11 test groups were created; 3 control groups were maintained at 35, 28 or 20 degrees C. Two additional groups, at each temperature, were exposed to 1.2 or 40 mumol/l propranolol. Developed force and effective refractory period (ERP) were measured. 3. At 35 degrees C, propranolol decreased developed force and lengthened ERP. At 28 degrees C, propranolol did not affect developed force, but ERP was lengthened. At 20 degrees C, 1.2 microM propranolol neither affected developed force or ERP, but 40 microM reduced developed force and lengthened ERP. CONCLUSION: hypothermia reduced propranolol's usual negative inotropic effect.

Adrenergic beta-Antagonists↗
PubMed2001

Effectiveness of propranolol for cocaine dependence treatment may depend on cocaine withdrawal symptom severity.

Propranolol may reduce symptoms of autonomic arousal associated with early cocaine abstinence and improve treatment outcome. This trial was an 8-week, double-blind, placebo-controlled trial of propranolol in 108 cocaine dependent subjects. The primary outcome measure was quantitative urinary benzoylecgonine levels. Secondary outcome measures included treatment retention, addiction severity index results, cocaine craving, mood and anxiety symptoms, cocaine withdrawal symptoms, and adverse events. Propranolol treated subjects had lower cocaine withdrawal symptom severity but otherwise did not differ from placebo treated subjects in any outcome measure. However, in a secondary, exploratory analysis, subjects with more severe cocaine withdrawal symptoms responded better to propranolol in comparison to placebo. In these subjects, propranolol treatment was associated with better treatment retention and lower urinary benzoylecgonine levels as compared with the placebo treatment. Propranolol may be useful only for the treatment of cocaine dependent patients with severe cocaine withdrawal symptoms.

Adolescent↗
PubMed1989

Quantification of propranolol enantiomers in small blood samples from rats by reversed-phase high-performance liquid chromatography after chiral derivatization.

A high-performance liquid chromatographic (HPLC) technique is described for quantification of R(+)- and S(-)-propranolol from 100-microliters rat blood samples. The procedure involves chiral derivatization with tert.-butoxycarbonyl-L-leucine anhydride to form diastereomeric propranolol-L-leucine derivatives which are separated on a reversed-phase HPLC column. The method as previously reported has been modified for assaying serial blood microsamples obtained from the rat for pharmacokinetic studies. An internal standard, cyclopentyldesisopropylpropranolol, has been incorporated into the assay and several derivatization parameters have been altered. Standard curves for both enantiomers were linear over a 60-fold concentration range in 100-microliters samples of whole rat blood (12.5-750 ng/ml; r = 0.9992 for each enantiomer). Inter- and intra-assay variability was less than 12% for each enantiomer at 25 ng/ml. No enantiomeric interference or racemization was observed as a result of the derivatization. No analytical interference was noted from endogenous components in rat blood samples. Preliminary data from two male Sprague-Dawley rats given a 2.0 mg/kg intravenous dose of racemic propranolol revealed differential disposition of the two enantiomers. R(+)-Propranolol achieved higher initial concentration but was eliminated more rapidly than S(-)-propranolol. Terminal half-lives of R(+)- and S(-)-propranolol were 19.23 and 51.95 min, respectively, in one rat, and 14.50 and 52.07 min, respectively, in the other.

Animals↗
PubMed1983

Electrophysiologic actions of high plasma concentrations of propranolol in human subjects.

The authors have previously shown that 40% of patients whose ventricular arrhythmias respond to propranolol require plasma concentrations in excess of those producing substantial beta-receptor blockade (greater than 150 ng/ml). However, the electrophysiologic actions of propranolol have only been examined in human beings after small intravenous doses achieving concentrations of less than 100 ng/ml. In this study, the electrophysiologic effects of a wider concentration range of propranolol was examined in nine patients. Using a series of loading and maintenance infusions, measurements were made at baseline, at low mean plasma propranolol concentrations (104 +/- 17 ng/ml) and at high concentrations (472 +/- 68 ng/ml). Significant (p less than 0.05) increases in AH interval and sinus cycle length were seen at low concentrations of propranolol, with no further prolongation at the high concentrations; these effects are typical of those produced by beta-blockade. However, progressive shortening of the endocardial monophasic action potential duration and QTc interval were seen over the entire concentration range tested (p less than 0.05). At high concentrations, there was significant (p less than 0.05) further shortening of both the QTc and monophasic action potential duration beyond that seen at low propranolol concentrations, along with a progressive increase in the ratio of the ventricular effective refractory period to monophasic action potential duration. No significant changes were seen in HV interval, QRS duration or ventricular effective refractory period. In summary, the concentration-response relations for atrioventricular conductivity and sinus node automaticity were flat above concentrations of 150 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1985

A randomized study comparing propranolol and diltiazem in the treatment of unstable angina.

One hundred consecutive patients hospitalized in the coronary care unit for unstable angina, excluding patients with Prinzmetal's variant angina, were randomized within 24 hours of admission to treatment with diltiazem (50 patients) or propranolol (50 patients). Also excluded were patients with previous coronary artery bypass surgery and those receiving a beta-receptor blocking agent at the time of hospital admission. Left ventricular function and the extent of coronary artery disease were similar in the two groups. During the hospital stay, the number of chest pain episodes decreased from a mean (+/- SD) of 0.75 +/- 0.1 per patient per day to 0.26 +/- 0.07 (p less than 0.05) with diltiazem and 0.29 +/- 0.1 (p less than 0.05) with propranolol therapy. The circadian distribution of chest pain episodes was affected similarly. After 1 month, 14 of the patients treated with diltiazem were symptom-free compared with 13 treated with propranolol. At a mean follow-up time of 5.1 months (range 1 to 15), death had occurred in two patients in each group and myocardial infarction in five diltiazem- and four propranolol-treated patients (difference not significant). Coronary artery bypass surgery had been performed in 21 diltiazem- and 19 propranolol-treated patients (difference not significant). Only 15 patients were symptom-free, 9 treated with diltiazem and 6 with propranolol. This similar result observed with the two forms of treatment suggests that coronary artery spasm may not be the main factor involved in unstable angina when Prinzmetal's variant angina is excluded. It also suggests that diltiazem can be used as an alternative to the usual treatment with beta-receptor blocking drugs.

Aged↗
PubMed1988

Use of exercise Doppler echocardiography to evaluate cardiac drugs: effects of propranolol and verapamil on aortic blood flow velocity and acceleration.

This study evaluated the ability of exercise Doppler echocardiography to identify hemodynamic changes due to cardiac medication. Twenty young healthy volunteers (mean age 30 years) underwent continuous wave Doppler examination from the suprasternal notch at rest, during each stage of a standard exercise protocol and immediately after exercise. On completion of the control test, each subject received either 60 to 80 mg of propranolol or 120 mg of verapamil orally, and the same exercise protocol was repeated after 90 min. During the control test, values for modal velocity, acceleration and flow velocity integral all increased significantly from baseline (p less than 0.0002 for each). When exercise was repeated after propranolol administration, values for all Doppler measurements were significantly altered. Modal velocity at baseline was significantly lower after propranolol when compared with control (0.53 +/- 0.11 versus 0.63 +/- 0.17 m/s; p less than 0.0001). Similarly, modal velocity at maximal exercise was significantly lower after propranolol (1.11 +/- 0.2 versus 1.25 +/- 0.21 m/s; p less than 0.0001). The effect of propranolol on acceleration was even greater, with blunting of baseline (11.4 +/- 2 versus 15.4 +/- 5 m/s per s; p less than 0.0005) and exertional (33.4 +/- 10 versus 56.3 +/- 15 m/s per s; p less than 0.0001) acceleration. The flow velocity integral during exercise was greater after propranolol (14.1 +/- 3.1 versus 10.1 +/- 3.2 cm; p less than 0.0005) than during the control test. Verapamil failed to influence any Doppler-measured index of aortic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1999

Microdialysis evaluation of the ocular pharmacokinetics of propranolol in the conscious rabbit.

PURPOSE: This study was conducted to assess the effects of anesthesia and aqueous humor protein concentrations on ocular disposition of propranolol. METHODS: Rabbits were anesthetized and a microdialysis probe was inserted into the anterior chamber of one eye; the contralateral eye served as a control. At timed intervals after probe placement, a 100-microl sample of aqueous humor was aspirated from each eye to determine protein concentration. In vitro protein binding parameters were used to simulate the impact of protein concentration on propranolol disposition. To assess the influence of anesthesia, probes were implanted in the anterior chamber of each eye. After >5-day stabilization, conscious and anesthetized rabbits (n = 3/group) received a 200-microg topical dose of [3H]DL-propranolol in each eye; propranolol was assayed in probe effluent. RESULTS: Changes in aqueous humor protein concentrations were observed following probe insertion. Simulations demonstrated that the unbound propranolol AUC (approximately 2.4-fold) in aqueous humor should be reduced due to protein influx. Intraocular propranolol exposure in anesthetized rabbits was approximately 8-fold higher than in conscious rabbits, and approximately 1.9-fold higher than in rabbits without a post-surgical recovery period. CONCLUSIONS: Anesthesia and time-dependent aqueous humor protein concentrations may alter ocular pharmacokinetics, and must be taken into account in the design of microdialysis experiments.

Adrenergic beta-Agonists↗
PubMed1980

Interaction between oral propranolol and hydralazine.

Seven healthy subjects were given oral propranolol (1 mg/kg) alone or in combination with hydralazine 25, 50, or 100 mg on separate occasions. Hydralazine induced variable increases in the peak concentrations (p less than 0.05) and in the area under the propranolol concentration: time curves (p less than 0.02) without change in the recovery of 14 C-propranolol/metabolites in urine or in the systemic clearance of propranolol; i.e., oral hydralazine enhanced the systemic availability of propranolol by alteration of "first-pass" (hepatic) clearance. The results indicate the possibility of change in presystemic clearance without reciprocal change in systemic clearance and also suggest that propranolol or any other high-clearance drug should be administered in fixed relationship to hydralazine and other drugs capable of altering "first-pass" hepatic extraction (either due to alteration in splanchnic blood flow or competitive inhibition of metabolism) if large variations in plasma concentrations are to be avoided.

Administration, Oral↗
PubMed1980

Propranolol dynamics in thyrotoxicosis.

Twenty-five thyrotoxic patients were treated with propranolol (160 mg/day) for 1 to 2 wk. Although the response to therapy varied there was a reduction (p less than 0.001) in supine and exercise heart rates and in sitting pulse rate. Serum triiodothyronine (T3) fell (p less than 0.001) and serum thyroxine did not change during propranolol therapy. Plasma propranolol levels before assessment varied from 5 to 121 ng/ml, and there were positive correlations between them and percentage reduction in exercise (r = 0.78, p less than 0.001) and resting (r = 0.61, n = 14, p less than 0.05) heart rates, percentage reduction in sitting pulse rate (r = 0.73, p less than 0.001), and the percentage reduction in serum T3 (r = 0.59, n = 23, p less than 0.01). Although weight loss ceased in the group as a whole the degree of continued weight loss or weight gain in individual patients was also related to plasma propranolol concentration (r = 0.61, p less than 0.01). The plasma propranolol level correlated (r = 0.62, p less than 0.01) with thyrotoxicosis therapeutic index. There was no correlation between degress of subjective improvement and plasma propranolol level.

Adolescent↗