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PubMed1981

Effect of propranolol on local cerebral blood flow under normocapnic and hypercapnic conditions.

The effect of propranolol (2.5 mg kg-1, i.v.) on local cerebral blood flow (CBF) in normocapnia was studied in rats maintained artificially ventilated on 70% N2O and 30% O2. The method used was autoradiography with [14C]iodoantipyrine. Although a single dose of propranolol, given 30 min prior to CBF measurements, somewhat reduced mean CBF values in all of the 22 structures analysed, none of the changes were significant. The results confirm previous ones, in which overall CBF was measured, in showing that beta-adrenergic mechanisms have little effect on normal cerebrovascular tone. Following a single dose of propranolol, results obtained in hypercapnia were equally negative; neither did CBF fall significantly when propranolol was given by constant infusion during 15 min. Furthermore, local CBF did not differ between animals infused with dl-propranolol and d-propranolol. It is concluded that in the rat, propranolol has but small effects on the CBF response to hypercapnia, if any. The results reveal that local CO2 responsiveness, calculated as delta CBF/delta PCO2, varies with normocapnic flow rates.

Animals↗
PubMed1990

Site of restoration of the effect of PTH by propranolol in respiratory alkalosis.

Respiratory alkalosis decreases the phosphaturic response to parathyroid hormone (PTH). beta-adrenoreceptor blockade by propranolol infusion restores the phosphaturic effect of PTH in respiratory alkalotic rats; however, the nephron site of these changes in phosphate reabsorption by propranolol is not known. The present study was performed to localize the nephron segment(s) involved in the restoration of the phosphaturic effect of PTH by propranolol infusion in respiratory alkalotic rats. PTH infusion increased the fractional delivery of phosphate (FDPi) to the late proximal tubule to similar levels in the propranolol and vehicle-infused respiratory alkalotic rats (FDPi 46.6 +/- 4.4% and 48.6 +/- 4.2%, respectively). In contrast, PTH only increased FDPi to the early distal tubules (to 17.1 +/- 0.9%) in the absence of propranolol compared to FDPi 41.9 +/- 2.5% in the presence of propranolol in respiratory alkalotic animals. We conclude that the restoration of the phosphaturic effect of PTH in respiratory alkalotic rats by propranolol infusion is due primarily to decreased reabsorption of phosphate by the straight segment of the proximal tubule.

Alkalosis, Respiratory↗
PubMed1997

The interaction between propranolol and the novel antimigraine agent zolmitriptan (311C90).

AIMS: Zolmitriptan (Zomig, formerly known as 311C90), a selective 5HT1B/1D agonist is under development as an acute oral treatment for migraine. Despite the use of prophylactic medication, such as propranolol, breakthrough attacks often occur in patients. Consequently we investigated the effects of propranolol on the pharmacokinetics of, and cardiovascular responses to, zolmitriptan. METHODS: A double-blind, randomized, crossover study of the effects of pre-treatment with propranolol 160 mg daily for 7 days or placebo on the pharmacokinetics and effects on blood pressure of a single 10 mg dose of zolmitriptan in 12 healthy volunteers. RESULTS: Propranolol increased mean zolmitriptan Cmax and AUC by 56% and 37% respectively; mean t1/2 was prolonged from 3.1 to 4.0 h. Mean Cmax and AUC of the pharmacologically active N-desmethyl metabolite were reduced by 24% and 11% respectively and the metabolite:parent AUC ratio (AUCm/AUCp) fell from 0.46 to 0.26. Mean Cmax and AUC for the inactive indole acetic acid metabolite were both reduced by 13% and AUCm/AUCp from 1.04 to 0.59. A small pressor effect of short duration was observed following zolmitriptan with mean peak rises of 13 and 11 mmHg in systolic and diastolic pressures respectively; propranolol had no effect on the pressor response. CONCLUSIONS: The results suggest that propranolol inhibits biotransformation of zolmitriptan but with no change in the small pressor response to zolmitriptan. It is therefore unlikely that the pharmacokinetic changes will lead to clinically important changes in pharmacological effects and dosage adjustment of zolmitriptan is not required in patients taking propranolol for migraine prophylaxis.

Adrenergic beta-Antagonists↗
PubMed1999

Effect of propranolol on central neurotransmitter release in Wistar rats analysed by brain microdialysis.

1. The effect of propranolol on amino acid neurotransmitter release in the rostral ventrolateral medulla (RVLM) was examined in urethane-anaesthetized male Wistar rats. 2. Amino acids released in the RVLM in response to intravenous administration of propranolol (0.4 mg/kg per min; n = 6) or nitroglycerin (0.02 mg/kg per min; n = 5) were determined by the brain microdialysis method. 3. Amino acids in dialysates were analysed by high-performance liquid chromatography and were quantified by ultraviolet absorbance. 4. Administration of both intravenous propranolol and nitroglycerin significantly decreased arterial blood pressure. Heart rate was decreased only by propranolol. 5. The reduction in arterial blood pressure produced by intravenous propranolol was accompanied by a decrease in the release of the excitatory amino acid glutamate in the RVLM. 6. The reduction in arterial blood pressure following intravenous nitroglycerin was not accompanied by a release of glutamate. 7. There were no significant changes in the levels of other amino acids (glycine, taurine, GABA) following either propranolol or nitroglycerin. 8. The decrease in glutamate release in the RVLM may account, in part, for the central depressor mechanism of propranolol.

Adrenergic beta-Antagonists↗
PubMed1991

Responders and non-responders to metoprolol, propranolol and nifedipine treatment in migraine prophylaxis: a dose-range study based on time-series analysis.

The aim of the present study was to ascertain, on the basis of single case statistics and time-series analysis, responder and non-responder rates for metoprolol, propranolol and nifedipine in migraine prophylaxis. In addition, an attempt was made to identify the dose relationship for the various drugs on headache parameters. In a double-blind dose-finding study, 58 patients were treated in five consecutive dosage steps each lasting 1-3 months. All patients kept a headache diary before, during and after treatment. Serum drug levels were also determined. The data were assessed by time-series analysis, as well as by multiple regression and analysis of variance. A significant improvement was noted in 54.4% of patients with migraine during treatment with metoprolol. The study did not confirm the high success rates in migraine prophylaxis of nifedipine and propranolol quoted in the literature. Administration of nifedipine led to an increase in migraine attacks in 71% of the patients. Nifedipine was of no value in the prophylaxis of migraine. Only 32% of patients showed a reduction in frequency of migraine attacks during administration of propranolol. The analysis of variance failed to show any significant difference between the responder rates for metoprolol and propranolol. Higher doses of propranolol and metoprolol were more effective. Multiple regression analysis explained a considerable part of variance for propranolol (but not for metoprolol) as a result of reduced intake of ergotamine preparations and analgesics. It can therefore be concluded that part of the prophylactic effect of propranolol is attributable to a reduction in the use of migraine medication.

Adolescent↗
PubMed1978

Renal plasma flow and cardiac output during hydralazine and propranolol treatment in essential hypertension.

Eleven patients with essential hypertension were given hydralazine (25 mg b.i.d.) for 2 weeks, hydralazine and propranolol (80 mg b.i.d.) for the next 2 weeks, and propranolol alone for the last 2 weeks. The changes in the renal and systemic circulation elicited by the drugs were studied before start of medication and bi-weekly during the treatment, using non-invasive radioisotope techniques. Hydralazine alone did not alter mean arterial blood pressure (MAP), heart rate (HR), cardiac index (CI), effective renal plasma flow (ERPF), peripheral renin activity (PRA) and plasma aldosterone (Aldo) but when propranolol was added MAP fell 15.2%, HR 22.5% and CI 18.4%, while ERPF was unchanged. When hydralazine was withdrawn and propranolol was given alone, ERPF decreased 13.2%. Plasma aldosterone was unchanged, whereas PRA decreased during propranolol treatment. The reduction in ERPF elicited by propranolol, was highly significant (P less than 0.01). From the test sequence it appears that dihydralazine prevents this effect of propranolol on kidney function. These findings might have a direct bearing on the choice of antihypertensive treatment.

Adult↗
PubMed1989

Nicardipine and propranolol in the treatment of essential hypertension.

Two hundred thirty-four patients with supine diastolic blood pressure of between 95 and 114 mm Hg were enrolled into a double-blind, randomized, parallel, multicenter trial. The patients were randomized to either nicardipine 30 mg tid, propranolol 40 mg tid, or nicardipine 30 mg tid and propranolol 40 mg tid for six weeks. Two hundred six patients yielded data for analyses. Of the 28 not included, seven had missing data, whereas the remaining 21 were excluded because they either failed to meet inclusion criteria or were noncompliant at endpoint. Both nicardipine and propranolol as monotherapies and in combination achieved statistically significant, (P less than .01), supine diastolic blood pressure reduction relative to baseline. The combination of nicardipine and propranolol showed a greater reduction in supine diastolic and systolic measurements than either of the monotherapies. Nicardipine produced greater blood pressure reductions one hour after dosing, whereas the propranolol treatment tended to produce slightly greater blood pressure decreases eight hours after dose. The combination always resulted in the greatest blood pressure reduction, independent of time after dose. Adverse experiences were reported by 26% of patients in the nicardipine-treated group, most often transient vasodilatory effects, by 17% of the propranolol-treated patients, and by 18% of the combination-treated group. This study demonstrated at the doses studied that nicardipine alone produced equivalent blood pressure reductions to those obtained by propranolol alone, but that the combination of these two drugs produced greater reductions in blood pressures than either of the monotherapies.

Adult↗
PubMed1994

Evaluation of the tumor-promoting activity of two beta-adrenoreceptor blocking agents, propranolol and atenolol, in liver of Fischer 344 rats.

The tumor-promoting activity of two beta-adrenoreceptor blocking agents, propranolol and atenolol, was tested in a two-stage protocol of hepatocarcinogenesis in male and female Fischer 344 rats. Propranolol is a lipophilic non-selective beta-blocker mainly eliminated via the liver; atenolol is a hydrophilic beta 1-selective blocking agent, mainly eliminated via the kidney. Animals were initiated with a single dose of diethylnitrosamine (DEN, 200 mg/kg, i.p.) and, after 17 days of recovery, were continuously treated with propranolol (75-100 mg/kg) or atenolol (300 mg/kg) by gavage for up to 21 months. Rats given phenobarbital (0.05% in the diet) were used as positive controls. After 2, 4 and 8 months of promotion, preneoplastic lesions were quantified by staining sections of liver for gamma-glutamyltranspeptidase (GGT). In non-initiated rats, neither propranolol nor atenolol influenced the development of spontaneous preneoplastic or neoplastic liver lesions. The results obtained in DEN-initiated rats given propranolol cannot be unequivocally interpreted. In the male, propranolol seemed to be ineffective. In the female, there was weak enhancement of DEN-induced GGT foci at 4 and 8 months and of neoplastic lesions thereafter. However, there was great interindividual variability in focus and tumor yields. Unfortunately, due to the high incidence of liver tumors in rats given DEN alone and the small number of propranolol-treated rats that survived until the end of the experiment, no definite conclusion can be drawn about the modifying potential of this beta-blocker on liver carcinogenesis. There was no evidence of liver tumor promotion in DEN-initiated rats of either sex given atenolol.

Animals↗
PubMed1981

Effects of propranolol on myocardial infarct size with and without coronary artery reperfusion in the dog.

The ability of propranolol to limit myocardial infarct size (IS) following coronary artery occlusion with and without reperfusion into a critical stenosis was assessed in the dog. IS was determined by the nitrobluetetrazolium staining method and expressed as percent of the left ventricle (free wall plus septum). In Series 1 dogs the left circumflex coronary artery (LCX) was ligated at its origin. IS at 6 h was similar in groups pretreated with saline (36.0 +/- 1.3%) or propranolol (0.2 mg . kg-1, 34.7 +/- 1.7%; 1.0 mg . kg-1, 36.7 +/- 1.5%; 4.4 mg . kg-1, 34.8 +/- 0.3%). In Series 2 dogs a relatively small infarction was produced by ligating the largest branch of the LCX between the left anterior descending and posterior descending arteries. IS at 6 h was not significantly different in dogs pretreated with saline (8.1 +/- 1.7%) or propranolol (0.2 mg . kg-1, 7.1 +/- 2.5%; 1.0 mg . kg-1, 4.6 +/- 1.2%). In Series 3 dogs the LCX was ligated approximately 10 mm from its origin for 60 min followed by reperfusion into a critical stenosis. IS determined at 24 h was significantly less in dogs treated with propranolol (1.0 mg . kg-1) before LCX occlusion (4.6 +/- 0.6%) or 5 min after LCX reperfusion (9.5 +/- 1.8%) than in dogs treated with saline (22.6 +/- 2.8%). In Series 4 dogs treatment was exactly as in Series 3 except that reperfusion was not instituted. IS was similar in dogs pretreated with saline (29.0 +/- 1.5%) or propranolol (31.1 +/- 3.0%). Thus, in the present study, propranolol limited IS in the presence but not in the absence of reperfusion. In the reperfusion model propranolol was effective when administered before coronary occlusion or after initiation of reperfusion.

Animals↗
PubMed1983

Severity of canine myocardial infarcts in relation to indices of oxygen demand: preservation of myocardial creatine kinase activity by vagal stimulation and propranolol.

The left anterior descending coronary artery was ligated in 58 open-chest anaesthetised dogs; 23 were controls, 15 were given intravenous propranolol 1 mg . kg-1 before and at 6 h intervals after coronary ligation, nine had bilateral cervical vagal nerve stimulation (VS) before and for 4 to 6 h after coronary ligation, and 11 had both VS and propranolol. None of the 20 dogs undergoing VS developed ventricular fibrillation within the first hour after coronary ligation compared to nine of the remaining 38 (P less than 0.05). Compared to controls, myocardial creatine kinase (CK) depletion in the epicardial layer of the infarct centre measured 24 h after coronary ligation was significantly less in the groups treated separately with vagal nerve stimulation and propranolol. Myocardial blood flow (MBF) measured at 15 min after coronary ligation was reduced to the normal myocardium by the interventions, but was unchanged at the infarct centre. Severely ischaemic myocardium (MBF less than or equal to 20% of normal) was better protected by the interventions than was moderately ischaemic myocardium. At 15 min after coronary ligation, the heart rate--blood pressure product (RPP) was reduced compared with controls by propranolol (18% reduction, P less than 0.05), reduced more by vagal stimulation (by 37%, P less than 0.001) and still more by vagal stimulation with propranolol (by 43%, P less than 0.001). Preservation of CK in myocardium with MBF less than or equal to 20% of normal was improved by VS and propranolol given separately roughly in proportion to reduction in RPP, but further reduction in RPP by VS and propranolol together did not improve CK levels further. We conclude that there may be an optimum level of indices of oxygen demand for preservation of very ischaemic myocardium in experimental infarction.

Animals↗
PubMed1989

Biochemical and morphological changes in myocardium during coronary occlusion and reperfusion in canine hearts: effects of propranolol on myocardial damage.

To clarify the mechanism of irreversible myocardial damage, we studied the relationship between ischaemic mitochondrial dysfunction and leakage of lysosomal enzymes, and the effects of propranolol on myocardial damage. Open chest anaesthetised dogs were divided into six groups: 30 min occlusion of the left anterior coronary artery (LAD); 2 h LAD occlusion; 2 h LAD occlusion after premedication with 0.3 mg.kg-1 propranolol; 30 min LAD occlusion/l h reperfusion; 2 h LAD occlusion/l h reperfusion; and 2 h LAD occlusion/l h reperfusion after propranolol premedication. After occlusion or reperfusion, heart mitochondria were prepared from normal and occluded or reperfused areas, and mitochondrial function (rate of oxygen consumption in State III, and respiratory control index) was measured polarographically. Myocardial tissue was fractionated and activities of lysosomal enzymes (N-acetyl-beta-glucosaminidase and beta-glucuronidase) were measured. Electron microscopic studies were performed. Thirty min occlusion induced mitochondrial dysfunction without leakage of lysosomal enzymes. Reperfusion for 1 h reversed these changes. However occlusion for 2 h induced mitochondrial dysfunction associated with the leakage of lysosomal enzymes, and mitochondrial dysfunction was not reversed by 1 h reperfusion. Propranolol reduced mitochondrial dysfunction after 2 h occlusion and prevented leakage of lysosomal enzymes. Mitochondrial function was fairly well maintained after 1 h reperfusion in dogs premedicated with propranolol. Structural changes in mitochondria were observed in the 2 h occlusion/l h reperfusion group, and were reduced by premedication with propranolol. These results suggest that irreversible injury of ischaemic mitochondria is closely linked with instability of lysosomal membranes, and that propranolol prevented irreversible myocardial mitochondrial dysfunction.

Animals↗
PubMed1984

Influence of propranolol plasma levels on hemodynamics during coronary artery bypass surgery.

Hemodynamic effects of propranolol during coronary artery surgery were investigated in 26 patients who chronically took propranolol and who received a standardized morphine/diazepam/pancuronium/halothane anesthetic. Effects were shown by correlating logarithm of the plasma propranolol concentrations versus percentage change in hemodynamics following stressful events (induction, intubation, skin incision, sternotomy, and sternal retraction). Log propranolol and hemodynamics following cardiopulmonary bypass also were correlated. A broad range of propranolol levels were observed. Levels (range and mean +/- SD) were preinduction 0-96 (25.6 +/- 21.6) ng/ml; preincision 0-86 (27.2 +/- 24.4) ng/ml; and sternal retraction 0-92 (28.2 +/- 25.4) ng/ml. The range of hemodynamic responses to stressful events also was broad. Representative changes between preincision control and sternotomy were (range and mean +/- SD): HR-8-30 (7 +/- 10) beats/min; PCWP 1-21 (8.5 +/- 4.6) mmHg; CI -0.2-1.1 (-0.2 +/- 0.7) 1 X min-1 X m-2, and SVR -244-1,288 (310 +/- 388) dyn X s X cm-3. By the time of sternal retraction, CI had declined from preincision values in 14 patients. Linear regression analysis demonstrated an inverse correlation between log propranolol and magnitude of HR, MAP, PCWP, and CI response to stressful stimulation. A direct but statistically weaker correlation with SVR also was seen. Significant correlations between log propranolol versus hemodynamic response to anesthetic induction and versus postcardiopulmonary bypass hemodynamics were not observed.

Adult↗
PubMed1987

Propranolol reduces bupivacaine clearance.

Propranolol reduces the clearance of lidocaine by both reducing hepatic blood flow and inhibiting lidocaine metabolism. The authors investigated the possibility that propranolol reduces the clearance of bupivacaine as well. Bupivacaine, 30-50 mg, was administered intravenously to six normal human volunteers, over 10-15 min on two occasions, at least 2 weeks apart. Propranolol, 40 mg orally every 6 h, was used on one occasion, beginning 24 h prior to the bupivacaine administration. The sequence of the sessions was randomized. Twenty-two venous blood samples were obtained over 36 h in order to determine bupivacaine clearance, terminal elimination rate constant, and volume of distribution. All subjects experienced mild CNS toxicity, consisting of tinnitus, facial tingling, or subtle visual disturbances, associated with peak venous plasma concentrations of 0.81 to 2.7 micrograms/ml. Mean bupivacaine clearance was 0.33 +/- 0.12 l/min for the control session and 0.21 +/- 0.12 l/min during propranolol use, a significant 35% reduction (P less than 0.01). The terminal elimination rate constant (beta) was 0.27 +/- 0.16 h-1 for the control session and 0.14 +/- 0.069 h-1 with propranolol (P less than 0.05); terminal elimination half-lives were 2.6 and 4.9 h, respectively. Volume of distribution was unchanged. Because bupivacaine clearance should be relatively insensitive to hepatic perfusion, it appeared that propranolol caused a substantial inhibition of bupivacaine metabolism at the level of the hepatocyte. These data suggest that concomitant use of propranolol could result in the accumulation of a toxic concentration of bupivacaine.

Adult↗
PubMed1987

Amrinone and verapamil-propranolol induced cardiac depression during isoflurane anesthesia in dogs.

This study was designed to investigate the possibility of whether verapamil diminishes the effects of amrinone, whether amrinone can reverse verapamil-propranolol depression, and also to evaluate whether the order of administering the drugs would have any effect during 1.7-1.8% end-tidal isoflurane anesthesia in dogs. At 3-4-week intervals, each of six conditioned mongrel dogs (23 +/- 1 kg) received amrinone (A) (4 mg/kg plus 100 micrograms X kg-1 X min-1), verapamil (V) (200 micrograms/kg plus 7.5 micrograms X kg-1 X min-1) and propranolol (P) (150 micrograms/kg plus 0.8 microgram X kg-1 X min-1) in four different orders of administration: VAP, AVP, VPA, and PVA. Plasma levels achieved were 15 +/- 1 to 24 +/- 2 micrograms/ml for amrinone, 24 +/- 2 to 59 +/- 10 ng/ml for propranolol, and 81 +/- 10 to 163 +/- 17 ng/ml for verapamil, equivalent to high therapeutic (amrinone) and therapeutic (propranolol, verapamil) levels in humans. The results of this study show that amrinone is able to reverse many of the effects of verapamil (group VAP) and also many of the effects of verapamil-propranolol or propranolol-verapamil (groups VPA, PVA) combinations. Amrinone improved cardiac index, left ventricular dP/dtmax, pulmonary capillary wedge pressure, and central venous pressure without increasing catecholamines. However, mean arterial pressure remained decreased with decreased systemic vascular resistance, which necessitates careful consideration depending upon patient circumstances. The results also show that verapamil-propranolol can reverse the positive inotropic effects of amrinone (group AVP).(ABSTRACT TRUNCATED AT 250 WORDS)

Amrinone↗
PubMedDate not supplied

Prolonged use of propranolol safely decreases cardiac work in burned children.

Propranolol has been shown to be effective for as long as 5 days in massively burned children to reduce heart rate and cardiac work. This article describes the use of propranolol given for 10 days to burned children to test whether the drug remains effective and safe in reducing heart rate and cardiac work for longer periods. We prospectively studied 22 children, 1 to 10 years of age with burns covering > or = 40% of their total body surface area. These children were treated with 0.5 to 1.0 mg/kg propranolol given orally or intravenously every 8 hours for 10 days. In both septic and nonseptic patients, propranolol significantly decreased their daily average heart rate (between 10% and 13%, p < 0.05) and rate-pressure product (between 10% and 16%, p < 0.05) compared with their 24-hour mean before propranolol treatment. No significant change in mean arterial blood pressure, or plasma urea nitrogen creatinine or glucose levels could be shown. No hypotension, hypothermia, azotemia, hyperglycemia or hypoglycemia, arrhythmia, bronchospasm, or peripheral ischemia was noted during or after treatment. Whereas propranolol lowered heart rate more per milligram per kilogram body weight when given intravenously, both routes were safe and effective. From these data, we conclude that propranolol can be given to decrease the work of the heart safely and effectively for > or = 10 days.

Administration, Oral↗
PubMed1989

Remodelling of the heart in DOCA-salt hypertensive rats by propranolol and by an alpha-2 agonist, rilmenidine.

The effects of rilmenidine [(N-dicyclopropylmethyl) amino-2-oxazoline; S 3341], an alpha 2 agonist, on the hypertensive rat heart have been compared with those of propranolol, using a model of deoxycorticosterone acetate (DOCA)-salt hypertension. One week after nephrectomy and initial treatment with DOCA-salt, which was continued for an additional 7 weeks, the two drugs were added to the rats drinking water at a concentration of 10 mg/kg per day for rilmenidine and 15 mg/kg per day for propranolol. Both drugs had a slight and similarly significant antihypertensive effect at their respective concentrations [systolic blood pressure in controls, 141 +/- 15 mmHg (n = 20); after DOCA-salt, 209 +/- 22 mmHg (n = 24); after propranolol, 182 +/- 19 mmHg (n = 20, P less than 0.01); after rilmenidine, 192 +/- 15 mmHg (n = 19, P less than 0.05)]. They also lowered the systolic blood pressure x frequency product (P less than 0.001). Propranolol, but not rilmenidine, significantly reduced the left ventricular weight: body weight ratio [in controls, 2.00 +/- 0.2 mg/g; after DOCA-salt, 3.04 +/- 0.5 mg/g; after propranolol, 2.67 +/- 0.4 mg/g (P less than 0.05); after rilmenidine, 3.13 +/- 0.6 mg/g (P = NS)]. However, both propranolol and rilmenidine reduced left ventricular weight [in controls, 676 +/- 57 mg; after DOCA-salt, 827 +/- 114 mg; after propranolol, 732 +/- 108 mg (P less than 0.01); after rilmenidine, 760 +/- 100 mg (P less than 0.05)].(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1999

Propranolol in prevention of portal hypertensive hemorrhage in children: a pilot study.

BACKGROUND: Data regarding the use of propranolol in the prevention of portal hypertensive hemorrhage in pediatric patients are limited despite its widespread use in adults with cirrhosis. The purpose of this study was to evaluate safety and efficacy of propranolol in the management of portal hypertension in the pediatric population. METHODS: Medical information was retrieved from the records of 21 children with portal hypertension who received propranolol either before or after an episode of gastrointestinal bleeding. Data collected included diagnosis, type of portal hypertension, age at initiation of therapy, bleeding episodes before and during propranolol therapy, degree of reduction of heart rate, adherence, and adverse effects. RESULTS: Fourteen of 21 patients did not experience portal hypertensive bleeding while receiving propranolol. Of the seven patients who had bleeding episodes, two had failed to adhere to the medication regimen, and four were receiving doses of less than 1 mg/kg per day. Only one of the four patients who experienced bleeding before initiation of therapy also bled while receiving propranolol, and two of the three patients who had a heart rate reduction of less than 25% each experienced a bleeding episode. Side effects were minimal and did not necessitate discontinuation of therapy in any patient. CONCLUSIONS: Propranolol was well tolerated with minimal side effects in our patients with portal hypertension. Adherence and adequacy of dosage (>1 mg/kg per day, more than twice daily dose frequency) are important determinants of efficacy. A reduction in heart rate of less than 25% may be associated with suboptimal efficacy.

Adolescent↗
PubMedDate not supplied

Effects of propranolol and timolol on calcium uptake by sarcoplasmic reticulum vesicles.

The effects of the beta-adrenergic receptor blocking agents propranolol and timolol on the initial calcium uptake velocity of sarcoplasmic reticulum vesicles of rabbit skeletal muscle were studied. Racemic d- and l-propranolol had similar inhibitory effects on initial calcium uptake velocity, which was inhibited 50% by 5--7 X 10(-4) M racemic propranolol. Timolol was a much less potent inhibitor of initial calcim uptake velocity; 50% inhibition occurred at approximately 10(-2) M timolol. Both drugs inhibited maximal calcium uptake velocity; however, KCa (the Ca2+ concentration at which calcium uptake was half-maximal) was modified differently. Propranolol increased KCa, whereas timolol caused the KCa to decrease. Addition of either drug to an ongoing calcium uptake reaction at the time that calcium content became maximal caused renewed calcium uptake. The relative potencies of propranolol and timolol as negative inotropic agents are similar to their potencies as inhibitors of sarcoplasmic reticulum calcium uptake, but dissimilar to their beta-adrenergic receptor blocking potencies. Timolol, which has been reported to have less negative inotropic effect than propranolol, is approximately 5 time more potent than propranolol as a beta-adrenergic receptor blocking agent but 15 times less potent as an inhibitor of sarcoplasmic reticulum calcium uptake. Inhibition of sarcoplasmic reticulum calcium uptake may thus characterize negative inotropic potencies of new beta-adrenergic receptor blocking agents.

Animals↗