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PubMed1985

A double-blind comparison of acebutolol (Sectral) and propranolol (Inderal) in the treatment of hypertension in black Nigerian patients.

Acebutolol and propranolol were compared in forty-five Black African patients in a double-blind randomized trial carried out at Ahmadu Bello University Teaching Hospital in Kaduna, Nigeria. After a wash-out period of 6 weeks, including placebo administration for the last 4 of those weeks, twenty-seven patients were given acebutolol once daily and eighteen were given propranolol twice daily for 12 weeks, followed by a tapering-off period of 2 weeks, making a total of 14 weeks on active treatment. The two beta-receptor blocking drugs were effective in controlling hypertension with final daily doses ranging from 160 to 320 mg in the propranolol group and 400 to 800 mg in the acebutolol group. The supine systolic blood pressure responses with acebutolol were statistically significant and better than those elicited by propranolol. Acebutolol produced less (resting) bradycardia than did propranolol; this may be related to acebutolol's intrinsic sympathomimetic activity. The only unpleasant side-effects reported in this study were slight dizziness in two patients treated with propranolol and slight tiredness in one patient treated with acebutolol. No significant abnormal changes were noted in laboratory tests or chest X-rays. Electrocardiography detected supraventricular tachyarrythmia in five patients: this disappeared by the end of the study. Acebutolol was shown to be a safe, effective and reliable antihypertensive drug, at least comparable to and probably slightly better than, propranolol in the treatment of hypertension in Black Nigerians. It has the added advantage of a once-daily dose schedule.

Acebutolol↗
PubMed1990

Propranolol and depression: evidence from the antihypertensive trials.

The relationship between propranolol and depression is a subject of controversy. Numerous case reports suggest that propranolol can cause depression, but two small prospective trials have failed to confirm this. The contemporary psychiatric literature is divided as to whether propranolol can cause depression. This study addresses this issue by re-analyzing side effect data from clinical trials of propranolol as an antihypertensive agent. A literature review was carried out and the data were analyzed using meta-analytic statistical techniques. Propranolol was found to cause depression as a side effect with a statistically greater frequency than the control medications used in these trials. As other side effects of propranolol include fatigue, diminished energy, decreased libido, anorexia and poor concentration, it is suggested that propranolol is a cause of organic mood disorder, depressed type.

Clinical Trials as Topic↗
PubMed1984

Once-daily propranolol for hypertension.

Twenty patients with essential hypertension, who were receiving a diuretic plus propranolol qid, were instructed to take their entire daily requirement of propranolol as a single morning dose. Blood pressure was measured in standing and supine positions at the end of a dosing interval. Patients were questioned about the occurrence of specific propranolol side effects during each of four bi-weekly evaluations. Mean blood pressure on once-daily propranolol did not differ significantly from that observed on propranolol qid. Daily doses of propranolol ranged from 80-320 mg. Side effects were infrequent and mild. We conclude that propranolol may be administered as a single daily dose to patients with hypertension whose blood pressure already has been controlled on a qid regimen.

Adult↗
PubMed1983

A double-blind comparison of indoramin and propranolol in the treatment of moderate to severe essential hypertension.

In a double-blind study, patients with moderate to severe essential hypertension were treated randomly with either indoramin or propranolol orally. The dose of both drugs was increased as necessary, to a predetermined level, in order to reduce the diastolic (Phase V) blood pressure to 100 mmHg or less. Patients were followed up for 12 weeks. There were 23 patients on propranolol and 27 on indoramin. The blood pressure in 22 patients on propranolol and 25 patients on indoramin was satisfactorily controlled in both the supine and standing positions. Mean supine blood pressure decreased from 181.3 +/- 14.2/116.2 +/- 6.8 mmHg to 140.6 +/- 7.1/95.7 +/- 3.6 mmHg after 12 weeks of treatment in patients receiving propranolol and from 188.3 +/- 18.9/118.4 +/- 8.7 mmHg to 144.7 +/- 7.3/95.7 +/- 2.5 mmHg in those treated with indoramin. There were no significant differences between the effects on supine and standing blood pressures and blood pressure control was maintained throughout the 12-week period in patients receiving indoramin and those receiving propranolol. Propranolol reduced the mean heart rate by approximately 16 beats/min in both the supine and standing positions. The maximum effect was seen 4 weeks after starting treatment and was maintained throughout the study. Sinus bradycardia (heart rate less than 60/min) occurred in 9 (39%) patients receiving propranolol. Indoramin caused a small but significant reduction in mean heart rate of approximately 4 beats/min in both the supine and standing positions. The maximum effect was seen after 2 weeks of treatment and was maintained for the rest of the duration of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Scale-up effects on dissolution and bioavailability of propranolol hydrochloride and metoprolol tartrate tablet formulations.

This study evaluated the effects of batch size on the in vitro dissolution and the in vivo bioavailability of immediate release formulations of propranolol hydrochloride and metoprolol tartrate. The formulations were manufactured as small and large batches (6 kg and 60 kg for propranolol; 14 kg and 66 kg for metoprolol), and dissolution was performed using USP Apparatus I at 100 rpm and pH 1.2. Two panels of 14 subjects each were randomly assigned to receive the small and large batches of either propranolol or metoprolol in an open, randomized single-dose study. Blood samples were collected over a 24-hour (propranolol) or 18-hour (metoprolol) period and analyzed by validated methods. As determined by the f2 metric (similarity factor), the dissolution of the small and large batches of propranolol and metoprolol was similar. The mean Cmax and AUC(inf) for the small batch of propranolol were 79.0 microg/L and 536 microg/L/hr, and for the large batch they were 83.5 microg/L and 575 microg/L/hr. Cmax and AUC(inf) for the small batch of metoprolol were found to be 95.5 microg/L and 507 microg/L/hr and for the large batch, 95.1 microg/L and 495 microg/L/hr. The 90% confidence intervals for the small and large batches were within the 80% to 120% range for lnCmax, and lnAUC(inf) for both the propranolol and metoprolol formulations. These results suggest that the scale-up process does not significantly affect the bioavailability of highly soluble, highly permeable drugs and in vitro dissolution tests may be useful in predicting in vivo behavior.

Adult↗
PubMed2003

The increased intestinal absorption rate is responsible for the reduced hepatic first-pass extraction of propranolol in rats with cisplatin-induced renal dysfunction.

The mechanisms responsible for the increased bioavailability of propranolol in renal dysfunction were investigated in rats. Experimental acute renal failure (ARF) was induced by intraperitoneal injection of cisplatin (5 mg kg(-1)). ARF induced a significant increase in blood propranolol concentration after intra-intestinal administration. The extent of bioavailability (F) of propranolol at an intestinal dose of 15 mg kg(-1) was 16.4% and 26.9% in control and ARF rats, respectively, and the F value at a 37.5 mg kg(-1) dose was 54.7% and 81.4% in control and ARF rats, respectively. In contrast, the blood propranolol concentration following intraportal infusion was not increased significantly in ARF rats. The hepatic first-pass extraction (E(h)) was dose-dependent and saturable: E(h) of propranolol in control rats was 58.0% and 18.3% at 8 and 20 mg kg(-1), respectively, and E(h) in ARF rats was 50.8% and 19.9% at 8 and 20 mg kg(-1), respectively. The initial absorption rate of propranolol from the intestine in ARF rats was significantly greater compared with control rats. These results indicated that the increased bioavailability of propranolol in rats with cisplatin-induced renal dysfunction was mainly a result of the increased absorption rate in the intestine followed by the partial saturation of hepatic first-pass metabolism.

Adrenergic beta-Antagonists↗
PubMed1985

Treatment of acute focal cerebral ischemia and recirculation with d-propranolol.

The purpose of the investigation was to evaluate the effects of d-propranolol upon temporary cerebral ischemia followed by a period of reperfusion, that is, a situation analogous to major cerebral artery embolization. Twenty adult cats, lightly anesthesized with nitrous oxide, underwent 4 hours of right middle cerebral artery (MCA) occlusion and 2 hours of recirculation. Ten cats were untreated and 10 cats received d-propranolol, the weak beta-blocking isomer of racemic (d,l) propranolol. The d-propranolol was infused directly into the right carotid artery at doses of 2 mg/kg, given as a bolus immediately before MCA occlusion, and 0.33 mg/kg/hour, given continuously for 6 hours beginning immediately after MCA occlusion. Systemic arterial blood pressure was similar in both groups, but heart rate was transiently reduced in the treated group immediately after the bolus injection of d-propranolol and MCA occlusion. Regional cerebral blood flow (rCBF), measured by the xenon-133 clearance technique, was not significantly different in the ischemic, right hemisphere. Electroencephalographic (EEG) activity changes in the ischemic, right hemisphere were similar in both groups, but there was significant deterioration of EEG activity in the left, nonischemic hemisphere of untreated cats after MCA reopening. Swelling of the ischemic, right hemispheres was similar in both groups and more severe than in previous studies wherein there was no recirculation phase. Carbon perfusion and blood-brain barrier changes were also similar. The results of the study failed to show a protective effect despite theoretical beneficial actions of d-propranolol. Also, the study demonstrated that d-propranolol does not have a detrimental effect upon rCBF in acute focal cerebral ischemia.

Animals↗
PubMed1981

Nonlinear first-pass metabolism of propranolol in the rat.

The mean hepatic extraction ratio (ER) of propranolol depending on the inflowing blood concentration to the liver was estimated directly by simultaneous measurements of arterial, hepatoportal, and hepatic venous blood concentrations of the drug following intravenous, intraportal, and intraduodenal administration in the rat. It was shown that the inflowing blood concentration to the liver caused considerable variation depending on the route of administration. The mean hepatic extraction ratio of propranolol in the first pass through the liver (ER)fipv and that of the drug after escaping the hepatic first-pass metabolism (ER)ripv were assessed by simultaneous administration of intraportal unlabelled propranolol and intravenous 14C-propranolol over a 50-min period. Consequently, a relation of (ER)fipv less than (ER)ipv less than (ER)ripv was observed in higher propranolol doses, if (ER)ipv refers to the overall mean hepatic extraction ratio following intraportal administration of propranolol. The fraction of orally administered dose reaching the systemic circulation for a drug exhibiting nonlinear hepatic first-pass metabolism was discussed. The unusual AUC-dose relationship of propranolol reported previously in the rat could be explained on the basis of both the nonlinear hepatic first-pass metabolism and the nonlinear hepatic metabolism of drug surviving the hepatic first-pass metabolism.

Animals↗
PubMed1983

Characterization of propranolol-induced relaxation of coronary artery.

Effects of propranolol on coronary artery were investigated in isolated dog coronary arteries and in isolated hearts of rats and guinea-pigs. Cumulative administration of dl-propranolol produced concentration-dependent relaxation of coronary arterial strips under potassium-contracture. There was no difference in relaxant potency between the optical isomers of propranolol. Lidocaine produced less relaxation than dl-propranolol, while atenolol and practolol scarcely affected the contraction. dl-Propranolol-induced relaxation was significantly restored by additional calcium or prevented by prior administration of calcium. In isolated hearts of rats and guinea-pigs which were perfused at a constant coronary inflow and paced at a constant rate, bolus administration of dl-propranolol produced dose-dependent falls in coronary perfusion pressure without significant changes in myocardial contractile force. Results indicate that propranolol may have relaxant activities on coronary arteries through inhibition of calcium influx in the cell membrane of coronary arterial smooth muscle.

Animals↗
PubMed2003

Effects of propranolol on xenobiotic enzyme activities in rat type II pneumocytes and alveolar macrophages in vivo.

The accumulation of basic drugs (cationic amphiphilic), such as beta-adrenergic antagonists, by pulmonary tissue is well known. Ring hydroxylation of nonselective beta-adrenergic blocking agent propranolol is mediated mainly by cytochrome P450 (CYP) 2D6 and N-desisopropylation by CYP1A2 in human and rat liver microsomes. In this study, the repeated administration of propranolol resulted in a marked inhibition of hepatic metabolism and an increase in its systemic availability, due to covalent binding of reactive metabolites (formed from 4-OH-propranolol) to liver microsomal P4502D enzymes. The absence of CYP1A2 and the presence of CYP2D in the lung suggest a different pulmonary metabolism of propranolol in comparison with those in the liver. In this study, we investigated its effects in vivo on some xenobiotic-metabolizing enzymes in rat type II pneumocytes (RTII) and rat alveolar macrophages (RAM). Twenty hours after the last multiple (7 days) oral administration, propranolol (100 mg/kg b.w.) decreased NADPH cytochrome c reductase activity and cytochrome P-450-dependent dealkylation of 7-benzyloxyresorufin (BROD) (CYP1A1, 2A1, 3A1) and 7-ethoxyresorufin (EROD) (CYP1A1) in RTII, while glutathione-S-transferase (GST), DT-diaphorase (QR), gamma-glutamyl transferase (gamma-GT) activities, intracellular reduced glutathione level and dealkylation of 7-pentoxyresorufin (PROD) (CYP2B1) were not changed. It was found that propranolol significantly increased NADPH cytochrome c reductase and BROD activities in RAM. The results suggest a different susceptibility of RTII and RAM to propranolol and its contrary effects on lung xenobiotic-metabolizing enzyme activities in both types of cells.

Adrenergic beta-Antagonists↗
PubMed1984

Nadolol compared to propranolol for treating chronic stable angina pectoris.

In order to determine the relative efficacy and dose equivalency of propranolol four times a day and nadolol once daily for the treatment of stable angina pectoris, ten patients were studied in a double blind randomized placebo controlled crossover study. Total daily doses of propranolol and nadolol were determined by titrating until an equivalent degree of reduction in the heart rate response to exercise was achieved. At these doses, the treadmill exercise time to 0.1 mV of electrocardiographic ST-segment depression was increased from 248 +/- 75 seconds on placebo to 405 +/- 56 seconds on propranolol (p less than 0.05) and 471 +/- 46 seconds on nadolol (p less than 0.01). Also, the mean frequency of angina decreased from eight attacks per week on placebo to three on propranolol and nadolol (both p less than 0.05). In six of the ten patients, the effective total daily dose of propranolol and nadolol was identical, and the dose ratio for all ten patients was 1.17:1, propranolol to nadolol. However, individual dose titration is recommended when switching from propranolol four times a day to nadolol once daily because of the dosage variability noted in 40 percent of the patients.

Adrenergic beta-Antagonists↗
PubMed1980

Changes of cyclic AMP concentration to isoproterenol after abrupt cessation of propranolol in rats.

Because the mechanism of adverse reactions to abrupt cessation of propranolol in patients with coronary heart disease was an enigma, we studied the effect of cessation of propranolol on beta-adrenergic receptor reactivity to catecholamine stimulation. The cyclic AMP concentrations in plasma and left ventricular muscle after the administration of isoproterenol (5 mg/Kg) were measured in rats before, during, 2 days after, and 4 days after of the administration of propranolol (5 mg/Kg). Two days after withdrawal from propranolol, the cyclic AMP concentrations in plasma and left ventricular muscle were significantly increased (p less than 0.005, p less than 0.01). Four days after withdrawal from propranolol, the cyclic AMP concentration in plasma was significantly increased (p less than 0.001). On the other hand, that of left ventricular muscle showed a tendency to have higher value, although, this was statistically not significant. From these results, this study suports that there is a hypersensitivity to adrenergic stimultion after abrupt cessation of long-term propranolol treatment. The explanation of propranolol withdrawal phenomenon most likely lies in lthe nature of beta adrenergic receptors that become activated during long-term blockade.

Animals↗
PubMed1983

Catecholamine sensitivity and cardiac myosin ATPase activity in dogs treated with propranolol.

The effects of propranolol treatment on adrenoceptor reactivity and on cardiac myosin ATPase activity have been studied. Eight mongrel dogs weighing 8 to 14 Kg were given propranolol orally 3 times daily (10 mg/Kg/day) for 2 weeks. Although the levels of propranolol were effective and there was a significant decrease in resting heart rate, there was no evidence of a rebound adrenoceptor hypersensitivity after abrupt withdrawal of propranolol treatment. The responsiveness of cardiovascular systems to 1-isoproterenol (1-ISO) was significantly attenuated 15 hrs after the last medication, but it did not differ from the premedication levels 6 days after discontinuation of medication. The effects of 1-ISO on adenylate cyclase activity in the myocardial membrane preparations were not significantly different between the 3 groups (no medication, 1 day and 6 days after discontinuation). With propranolol treatment, though a rise in total plasma catecholamine (norepinephrine, epinephrine, dopamine) levels was the predominant change, there were no definite changes in respective catecholamines. Serum triiodothyronine (T3) increased during medication in 7 of the 8 animals and decreased after medication. Calcium-activated and K+-activated myosin ATPase activity in the inner and outer layers of the left ventricular wall were uniform in unmedicated dogs, and propranolol produced no significant effects. No reliable evidence for propranolol withdrawal syndromes was provided in the present study.

Adenosine Triphosphatases↗
PubMed1994

Pharmacokinetics of propranolol used for suppressing tachycardia in hyperthyroidism.

The aim of this study was to investigate the pharmacokinetics of propranolol in patients with hyperthyroidism, and its effect on heart rate (HR) using 24 hour-ECG monitoring. Subjects included 9 patients with hyperthyroidism (group H) and 9 euthyroid patients with hypertension selected as the control group (group C). All patients took propranolol at a dosage of 10 mg, 3 times a day for 7 days. Plasma propranolol concentrations were measured on the 7th day of its administration by the HPLC method. Twenty-four hour-ECG monitoring was recorded twice before and after treatment with propranolol. The mean reduction in the minimum HR was 10.7 +/- 3.6 (11.9 +/- 3.6%) in group H and 5.0 +/- 1.6 (9.5 +/- 3.0%) bpm in group C. That in the average HR was 12.2 +/- 3.7 (11.3 +/- 3.1%) in group H and 9.2 +/- 2.2 bpm (13.7 +/- 3.2%) in group C. That in the maximum HR was 16.9 +/- 5.2 (10.9 +/- 3.1%) in group H and 24.4 +/- 2.4 bpm (21.9 +/- 2.1%) in group C. The peak concentration of propranolol in plasma was 10.8 +/- 2.4 ng/ml in group H and 55.3 +/- 14.3 ng/ml in group C (p < 0.01). There was a linear correlation between the reduction in the hourly maximum heart rate and the peak plasma propranolol concentration in group H. Cardiovascular manifestations in hyperthyroid patients were related to sympathetic hypersensitivity and their improvement was not fully obtained by small doses of propranolol.

Adult↗
PubMed2006

Different effects of propranolol, phenylephrine, and saline volume loading on catecholamine-induced left ventricular outflow tract obstruction in acute coronary syndrome.

Hemodynamic deterioration due to left ventricular outflow tract (LVOT) obstruction can occur during catecholamine infusion in patients with acute coronary syndrome (ACS). The purpose of the present study was to compare the utility of propranolol, phenylephrine infusion, and rapid saline loading for reversal of dobutamine-induced LVOT obstruction in a canine model of ACS. ACS was induced via left anterior descending artery ligation in 21 open-chest anesthetized dogs, and LVOT obstruction, defined as an LVOT gradient > 30 mmHg, was induced by dobutamine infusion (20 to 40 microg/kg/min). Subsequently, the effects of propranolol infusion (0.7 to 1.0 microg/kg/min, n = 8), phenylephrine infusion (10 to 200 microg/kg/min, n = 7), and saline loading (200 to 400 mL/hr, n = 6) were assessed by serial hemodynamic measurements. All interventions produced significant and comparable improvements in the LVOT pressure gradient (propranolol: 60 +/- 16 to 15 +/- 12; phenylephrine: 68 +/- 15 to 12 +/- 10; saline loading: 58 +/- 18 to 22 +/- 10 mmHg; P < 0.001 for baseline versus postintervention; P = NS for comparison between interventions). Phenylephrine produced the greatest elevation in aortic pressure (propranolol: +15 +/- 13; phenylephrine: +51 +/- 36; saline loading: +15 +/- 15 mmHg; P < 0.05), while saline loading produced the greatest increase in cardiac output (propranolol: +0.05 +/- 0.12; phenylephrine: +0.28 +/- 0.37; saline loading: +0.73 +/- 0.48 L/min; P < 0.05). Propranolol was the only intervention that produced a significant decrease in diastolic pulmonary artery pressure (16 +/- 5 to 11 +/- 3 mmHg, P < 0.05). Propranolol, phenylephrine infusion, and saline volume loading were similarly effective in reversing dobutamine-induced LVOT obstruction in this canine model of ACS. However, each intervention produced different hemodynamic effects with potentially different clinical indications.

Adrenergic beta-Antagonists↗
PubMed1976

Pharmacokinetics and effects of propranolol in terminal uraemic patients and in patients undergoing regular dialysis treatment.

Propranolol blood and plasma levels were measured after a single oral dose of 40 mg in patients with chronic renal failure, in patients undergoing regular dialysis treatment, and in healthy volunteers. Peak levels were observed in all cases within 1.5 to 3 hours. However, peak blood and plasma concentrations of propranolol in the chronic renal failure group were 2- to 3-fold higher (161 +/- 41 ng/ml) than those observed in the dialysis patients (47 +/- 9 ng/ml) and in the healthy volunteers (26 +/- 1 ng/ml). The apparent plasma clearance was also significantly reduced in the patients with chronic renal failure. The data suggest a reduced hepatic extraction in chronic renal failure patients. A significant increase in the fraction of the dose available to the systemic circulation was also found, together with a modification of apparent plasma half-life and volume of distribution in regular dialysis patients during the dialysis day as compared with the after-dialysis day. No extraction of propranolol by the dialyzer was noticed. Marked fluctuations in propranolol blood concentrations were also observed in patients on regular dialysis following continuous propranolol treatment. The suppressive effect of propranolol on plasma renin activity did not fully correlate with the hypotensive effect of the drug. On the basis of the reported data, propranolol should be used with great caution and at low doses in chronic renal failure.

Adult↗
PubMed1990

Pharmacokinetics and metabolism of oral doses of a 4'-methylthio derivative of propranolol in man.

1. The objective of this study was to determine the oral dose pharmacokinetics and metabolism of 4'-methylthiopropranolol (MTP) in man and compare the results with observations for propranolol in previous studies. 2. Three women and five men received single oral doses of MTP, dose range 5-320 mg. Plasma concentration of MTP over time were measured by gas chromatography-mass spectrometry. MTP metabolites in urine were identified by comparative high-performance liquid chromatographic (HPLC) retention times and mass spectrometry with previously characterized reference compounds and quantified by HPLC. 3. The oral clearance of MTP of 1.2-1.4 l/min for the 80, 160 and 320 mg doses was about one third of the value previously reported for propranolol. The half-life for MTP (3.3-4.1 h) was, however, similar to that of propranolol. In contrast to propranolol, the peak (2.5 h) plasma concentrations of MTP increased linearly with dose (5-320 mg). 4. The oral clearance for MTP was about 2-fold higher in the men than in the women (P less than 0.01). In addition, the clearance of the (S)-enantiomer was about 30% higher than that of the (R)-enantiomer (P less than 0.05), which was a reversal of that seen with propranolol. 5. The metabolism of MTP resulted mainly in sulphur oxidation to sulphoxide and sulphone metabolites. These two metabolites accounted for 75% of the MTP dose. This switching from aromatic carbon oxidation for propranolol to sulphur oxidation for MTP is proposed as the basis of the lower oral clearance of MTP. 6. This study also demonstrated higher plasma binding of MTP (unbound fraction 3.7%) than of propranolol (10.5%; P less than 0.01), a factor probably contributing to decreased tissue distribution of MTP.

Administration, Oral↗
PubMed2003

Meta analysis of propranolol effects on gastrointestinal hemorrhage in cirrhotic patients.

AIM: To assess the effects of propranolol as compared with placebo on gastrointestinal hemorrhage and total mortality in cirrhotic patients by using meta analysis of 20 published randomized clinical trials. METHODS: A meta analysis of published randomized clinical trials was designed. Published articles were selected for study based on a computerized MEDLINE and a manual search of the bibliographies of relevant articles. Data from 20 relevant studies fulfilling the inclusion criteria were retrieved by means of computerized and manual search. The reported data were extracted on the basis of the intention-to-treat principle, and treatment effects were measured as risk differences between propranolol and placebo. Pooled estimates were computed according to a random-effects model. We evaluated the pooled efficacy of propranolol on the risk of gastrointestinal hemorrhage and the total mortality. RESULTS: A total of 1,859 patients were included in 20 trials, 931 in the propranolol groups and 928 as controls. Among the 652 patients with upper gastrointestinal tract hemorrhage, 261 patients were treated with propranolol, and 396 patients were treated with placebo or non-treated. Pooled risk differences of gastrointestinal hemorrhage were -18 % [95 % CI, -25 %, -10 %] in all trials, -11 % [95 % CI, -21 %, -1 %] in primary prevention trials, and -25 % [95 % CI, -39 %, -10 %] in secondary prevention trials. A total of 440 patients died, 188 in propranolol groups and 252 in control groups. Pooled risk differences of total death were -7 % [95 % CI, -12 %, -3 %] in all trials, -9 % [95 % CI, -18 %, -1 %] in primary prevention trials, and -5 % [95 % CI, -9 %, -1 %] in secondary prevention trials. CONCLUSION: Propranolol can markedly reduce the risks of both primary and recurrent gastrointestinal hemorrhage, and also the total mortality.

Adrenergic beta-Antagonists↗