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PubMed2002

Propranolol decreases splanchnic triacylglycerol storage in burn patients receiving a high-carbohydrate diet.

OBJECTIVE: To quantify the various components of splanchnic free fatty acid and very-low-density lipoprotein-triacylglycerol (VLDL-TAG) metabolism in order to gain insight into the mechanisms responsible for the development of fatty liver in severely burned patients, and to determine if decreasing free fatty acid availability by use of propranolol could potentially reduce hepatic fatty acid accumulation. SUMMARY BACKGROUND DATA: Hepatic fat accumulation results from an imbalance between fatty acid uptake, oxidation, and release via VLDL-TAG. Fatty acid delivery is accelerated in burn patients because of stimulated lipolysis. Since propranolol decreases lipolysis, it should also decrease hepatic fatty acid uptake and thus TAG synthesis. METHODS: Stable isotope-labeled tracers and regional catheterization enabled quantification of various parameters of lipid metabolism across the splanchnic bed in severely burned patients. The acute effects of propranolol treatment were studied in all patients, and in a subgroup of patients the chronic (3 weeks) effects of propranolol were assessed. RESULTS: The rate of splanchnic uptake of palmitate was 1.68 +/- 1.3 micromol/kg/min, whereas the rates of oxidation and VLDL-TG secretion were only 0.12 +/- 0.11 and 0.003 +/- 0.02 micromol/kg/min, respectively. Propranolol significantly reduced palmitate delivery, and thus palmitate uptake, without significantly affecting oxidation or VLDL-TAG secretion. Thus, palmitate storage was reduced from 1.53 +/- 1.30 micromol/kg/min without propranolol to 0.76 +/- 0.58 micromol/kg/min after propranolol. CONCLUSIONS: Hepatic fat storage in burn patients is due to low rates of both fatty acid oxidation and VLDL-TAG secretion. Propranolol can decrease hepatic fat storage by limiting fatty acid delivery.

Adolescent↗
PubMedDate not supplied

Effects of propranolol administration on cardiac responses to burn injury.

Previous studies showing that propranolol upregulates beta-adrenergic receptors and protects against myocardial ischemia led us to hypothesize that preburn propranolol would protect against postburn cardiac dysfunction. Guinea pigs were treated with propranolol 3 mg/kg/day for 14 days, then deeply anesthetized and subjected to a 45% 3 degrees scald burn; eight guinea pigs treated with propranolol served as the control group (group 1). Burned guinea pigs were resuscitated with Ringer's lactate given as either 4 ml (group 2, N = 8), 6 ml (group 3, N = 10), or 8 ml (group 4, N = 6) per kg/% burn. Guinea pigs treated for 14 days with vehicle (water) were subjected to either sham burn (non-propranolol control, group 5, N = 10) or burn and treatment (group 6, N = 10) as described for group 2. Fluid resuscitation in non-propranolol-treated guinea pigs failed to overcome burn-induced cardiac deficits, as indicated by significantly lower left ventricular pressure, 86 +/- 2 versus 62 +/- 3 mm Hg; +dP/dt max, 1365 +/- 43 versus 1110 +/- 44 mm Hg/sec; -dP/dt max, 1184 +/- 31 versus 881 +/- 40 mm Hg/sec, p < 0.001. Burn-mediated cardiac defects occurred in all propranolol-treated guinea pigs regardless of the fluid volume given. Our data show that (1) propranolol did not protect against burn-induced cardiac dysfunction, and (2) chronic beta-adrenergic blockade increases postburn fluid requirements for maintenance of cardiodynamic stability and for survival.

Animals↗
PubMed1988

Comparison of quality of life on nitrendipine and propranolol.

A multicenter, randomized, double-blind, comparative study was conducted in 274 patients with mild to moderate hypertension to assess the impact of nitrendipine and propranolol on quality of life. After placebo baseline, 136 patients were given nitrendipine (5-20 mg b.i.d.) and 138 were given propranolol (40-120 mg b.i.d.). Quality of life was evaluated at baseline, weeks 6-10, and weeks 14-18 of the maintenance period. At weeks 6-10, the nitrendipine group became significantly more vigorous (p less than 0.01) and less fatigued (p less than 0.05) than the propranolol group. Propranolol subjects noted decreased problems of trembling hands (p less than 0.01) and alcohol use (p less than 0.05) than the nitrendipine subjects. No other significant differences between groups in mood states, troublesome conditions (insomnia, headaches, and loss of appetite), or sexual satisfaction were noted at this visit, and patient willingness to continue study medication was marginally significantly higher (p less than 0.1) in the nitrendipine group than in the propranolol group. At weeks 14-18, the propranolol subjects perceived significantly decreased problems with the "felt worried, tense, and drank alcohol to cope" factor (p less than 0.05); however, there were no differences between groups at this visit for Profile of Mood States (POMS) scores, sex life variables, or medication preference. Based on within-group analysis, the propranolol group perceived a reduction in partner sexual satisfaction (p less than 0.05). Overall, nitrendipine seemed to be better tolerated than propranolol.

Adult↗
PubMed1990

Effect of propranolol on diastolic time during exercise.

To evaluate the effect of propranolol on diastolic time (DT) during uninterrupted upright exercise, 11 men with normal coronary arteries receiving oral propranolol and 10 men with coronary artery disease (CAD) were studied by ear densitography. The DT-heart rate (HR) regression equation during exercise obtained from persons without CAD receiving propranolol was DT = e(6.923-0.014 X HR), which was not statistically different compared to that of normal volunteers with no medication. All 10 men with CAD had ischemic electrocardiographic responses at peak exercise with no medication but had no signs of ischemia during exercise after receiving oral propranolol therapy. Although propranolol caused no significant difference in the DT-HR relation in patients with CAD at 1-min exercise, a significant difference in the DT-HR relation was observed after propranolol therapy at peak exercise. In addition to negative chronotropic action (leftward shift along the DT-HR curve), prevention of disproportionate DT shortening at peak exercise (upward shift of the DT-HR curve) with propranolol through its beneficial action on myocardial ischemia tends to increase myocardial perfusion in patients who, when off propranolol, had ischemic response to exercise.

Adult↗
PubMed1978

(+)-Propranolol clearance, an estimation of hepatic blood flow in man.

1 Hepatic blood flow was determined before and during (+)- and (+/-)-propranolol plasma concentration plateaus in 19 patients with suspected renal hypertension and normal liver function. 2 Hepatic blood flow significantly decreased (P less than 0.001) during (+/-)-propranolol administration and remained unchanged during (+)-propranolol administration. 3 Hepatic extraction ratio was 74 +/- 1% (+/-)-propranolol and 79 +/- 2% for (+)-propranolol. 4 Total propranolol clearances were determined during the steady-state achieved by a constant infusion. A highly significant positive relationship was observed (r = +0.86; P less than 0.01) between hepatic blood flow and (+)-propranolol clearance. The slope of the curve was 1.05 +/- 0.27. 5 The result implies that the total clearance of (+)-propranolol constitutes an accurate estimation of basal hepatic blood flow in subjects with normal liver function.

Adult↗
PubMed1980

Propranolol disposition in renal failure.

1 Previous studies of propranolol disposition in renal failure have been conflicting. 2 Using simultaneous administration of [3H]-propranolol intravenously and unlabelled propranolol orally the principal determinants of drug distribution were calculated in normals, patients with severe renal impairment (creatinine clearance 14.5 +/- 2.8 ml/min) but not on haemodialysis and patients on haemodialysis (creatinine clearance less than 5 ml/min). 3 The effect of haemodialysis on propranolol binding and free fraction was also examined. The percentage of propranolol unbound rose from 7.1% to 9.9%. (P less than 0.001) 20 min following heparinization and beginning haemodialysis. This was accompanied by a large rise in free fatty acids from 0.567 +/- 0.059 to 3.326 +/- 0.691 mumol/ml (P less than 0.005). 4 The blood to plasma concentration ratios of propranolol were significantly higher in patients with renal failure (P less than 0.02) and on haemodialysis (P less than 0.001) and were significantly negatively correlated (P less than 0.001) with the haematocrit. 5 Although the half-life propranolol was significantly shortened in the patients with renal failure (P less than 0.02), there was no change in the apparent liver blood flow, extraction ratio or the principal determinants of steady-state drug concentrations in blood namely oral and intravenous clearance from blood. 6 There is, therefore, no pharmacokinetic basis to adjust the dosage of propranolol in patients with renal failure.

Administration, Oral↗
PubMed1983

Induction of propranolol metabolism by rifampicin.

The effect of rifampicin on the blood concentration-time curve of propranolol at steady-state following oral administration of 120 mg every 8 h was investigated in six normal, young, male subjects. After an initial 2 week dosing period, all individuals additionally received 600 mg rifampicin daily for 3 weeks followed by a 4 week period during which again only the propranolol was given. In four of the subjects the effects of 900 and 1200 mg rifampicin daily was also studied. Changes in disposition were assessed by estimation of propranolol's oral clearance and elimination half-life during the dosage interval. Rifampicin (600 mg/day) caused a large increase in propranolol's oral clearance (35.7 +/- 16.3 vs 96.1 +/- 26.9 ml min-1 kg-1, mean +/- s.d.), but neither the elimination half-life nor extent of plasma binding were affected. Increasing the daily dosage to 900 and 1200 mg did not cause any additional changes in oral clearance. Four weeks after discontinuing rifampicin, propranolol's oral clearance had essentially returned to its pre-induction level. The oral clearance of propranolol was significantly smaller (89.5 +/- 14.4%) during the dosage interval immediately after administration of the last rifampicin dose than the value measured 24 h later. The findings are consistent with rifampicin causing induction of the drug metabolizing enzymes responsible for propranolol's biotransformation. The marked reduction in the steady-state propranolol blood concentration that results from chronic rifampicin administration would be expected to result in a significant change in clinical effectiveness of the beta-adrenoceptor blocker when the two drugs are used concurrently.

Adult↗
PubMed1984

The effects of acute or chronic ingestion of propranolol or metoprolol on the metabolic and hormonal responses to prolonged, submaximal exercise in hypertensive men.

We have studied the effects of single oral doses of, and of 28 days treatment with, placebo, propranolol or metoprolol, on the metabolic and hormonal responses to prolonged exercise in hypertensive men. Blood glucose levels fell during exercise on all occasions. No additional effects of the beta-adrenoceptor antagonists, compared to placebo, were observed. The exercise-induced increase in plasma potassium was enhanced after a single dose of propranolol or metoprolol, and also after chronic treatment with propranolol. Chronic treatment with either drug led to an increase in plasma potassium levels at rest. The growth hormone response to exercise was potentiated by a single dose of metoprolol or propranolol, and after chronic treatment with the drugs. A single dose of propranolol (but not metoprolol) was associated with a marked increase in plasma cortisol and adrenaline levels during exercise. After chronic treatment no such increase occurred. In both the acute and chronic phases of the study, blood lactate levels were higher during exercise in the presence of either propranolol or metoprolol compared to placebo, whereas non-esterified fatty acid levels were lower. A single dose of metoprolol produced a significantly greater reduction in blood glycerol levels during exercise than a single dose of propranolol. After chronic treatment, both propranolol and metoprolol produced similar reductions in blood glycerol levels during exercise. After a single dose, both drugs significantly augmented the increase in plasma noradrenaline levels during exercise. A similar effect was seen after chronic treatment.

Blood Glucose↗
PubMed1984

Stable oral availability of sustained release propranolol when co-administered with hydralazine or food: evidence implicating substrate delivery rate as a determinant of presystemic drug interactions.

A study was made of the influence of hydralazine on the oral availability of a sustained release formulation of propranolol (Inderal LA). Sustained release propranolol 160 mg was given orally either alone or in combination with oral hydralazine 25 mg on separate occasions to six healthy volunteers. Blood and urine samples were collected post-dosing over 34 h. Peak concentrations of propranolol, time to peak and area under the plasma concentration-time curve (AUC) were not altered by co-administration of hydralazine with sustained release propranolol. Similarly, there was no change in recovery of 11C-labelled propranolol and metabolites in those individuals to whom tracer label was given. These results contrast with previous reports of marked interaction between the conventional formulation of propranolol and hydralazine or food. Interactions were confirmed between hydralazine and conventional propranolol in three subjects who had been studied previously with sustained release propranolol. Analysis of metabolite profiles in one of these subjects established that the major metabolites do change under hydralazine stimulus. These results indicate that substrate delivery rates may determine presystemic drug interactions, suggesting capacity limitations of hydroxylation processes or short-term flow redistribution following hydralazine, resulting in functional shunting past the hydroxylation enzymes. These results exclude global or lasting enzyme inhibition by hydralazine or simple flow-sensitivity of presystemic clearance.

Adolescent↗
PubMed1986

Pharmacodynamics and pharmacokinetics of single doses of ketanserin and propranolol alone and in combination in healthy volunteers.

The potential interaction between ketanserin and propranolol has been investigated in eight healthy volunteers. Volunteers received single doses of placebo, propranolol (80 mg), ketanserin (20 mg), and propranolol (80 mg) plus ketanserin (20 mg) following a randomised double-blind regimen. A single dose of ketanserin had little effect on resting heart rate and blood pressure and the effects of propranolol and ketanserin in combination were similar to those of propranolol alone. The inhibition of exercise induced tachycardia by propranolol was not affected by ketanserin. The pharmacokinetics of propranolol elimination were not influenced by the concurrent administration of ketanserin, nor the pharmacokinetics of ketanserin by propranolol.

Adult↗
PubMed1992

Lack of effect of ageing on the stereochemical disposition of propranolol.

The elderly are more resistant to the effects of propranolol than the young. To determine whether the decreased sensitivity in the elderly could be due to stereoselective alteration in propranolol metabolism, we investigated the effect of age on the oral clearance of (-)- and (+)-propranolol. Six young (aged 24-32, mean 27.3 +/- 1.3 years) and six elderly (65-80, mean 71.3 +/- 2.7 years) white male volunteers were given a single 80 mg oral dose of racemic propranolol. The mean peak plasma concentrations of both (+)- and (-)-propranolol were significantly higher (P less than 0.05) in the elderly (105.7 +/- 19.7 and 165.0 +/- 29.7 nmol l-1) compared with the young subjects (68.6 +/- 10.1 and 115.7 +/- 18.1 nmol l-1). The oral clearances of both (+)- and (-)-propranolol were significantly higher (P less than 0.05) in the young (6933 +/- 598 and 4554 +/- 372 ml min-1) than in the elderly (4548 +/- 712 and 2941 +/- 473 ml min-1). Age had no effect on the relative concentration of the two isomers. Thus, the ratio of (+)-propranolol to (-)-propranolol was 0.67 +/- 0.05 in the young compared with 0.65 +/- 0.02 in the elderly.

Adult↗
PubMed1988

High-performance liquid chromatographic determination of propranolol and 4-hydroxypropranolol in serum.

A simple, sensitive and selective high performance liquid chromatographic method for the analysis of propranolol and its major metabolite 4-hydroxypropranolol is developed. The drugs and the internal standard, quinidine, were extracted from serum with ether at pH 10. The latter was evaporated and the residue was dissolved into phosphoric acid solution. Propranolol, 4-hydroxypropranolol and quinidine were eluted from 5 microns, C-18 reversed phase column with a mobile phase consisting of acetonitrile-methanol-phosphoric acid at pH 4 and detected with fluorescence detector. Quantification was achieved by measuring the peak height ratio of each drug to the internal standard. Interference due to either biological constituents of serum or other propranolol metabolites such as n-desisopropyl propranolol and propranolol glycol was absent. The mean percentage recoveries for serum samples spiked with propranolol and 4-hydroxypropranolol were 94.7 and 98.4%, respectively. Detection limits were 10 ng/ml for propranolol and 5 ng/ml for 4-hydroxypropranolol. Within-day coefficients of variation ranged from 3.2-6.9% for propranolol and 0.8-6.2% for 4-hydroxypropranolol.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Effects of propranolol on development and maintanance of severe renal hypertension in rats.

1. The effect of chronic administration of propranolol on the development and maintenance of severe renal hypertension in rats subjected to unilateral renal artery constriction was studied in relation to possible changes in peripheral PRA and the blood and tissue levels of propranolol. Propranolol was administered s.c. twice daily in doses of 1, 10 and 25 mg/kg, starting 2 days before operation. 2. Contrary to expectations, not only did the initial rise in systolic blood pressure become accelerated, but the established level of hypertension attained in the propranolol treated rats was of the same severity as that attained in placebo treated rats. Moreover, the progressive rise in peripheral plasma renin activity following unilateral renal artery constriction was not affected by propranolol administration. 3. The same doses of propranolol were also administered daily for 8 days to rats with established severe hypertension. A slight further rise in blood pressure occurred initially, followed by a moderate decrease of 15-25 mmHg. Propranolol failed to exert this minor hypotensive effect in hypertensive rats treated concomitantly with furosemide. No suppressive effect on the markedly increased levels of plasma renin activity was observed in these severely hypertensive rats in the presence or absence of furosemide administration. 4. These results indicate that in severely renal hypertensive rats propranolol has only a minor hypotensive effect and no blocking action on renin release under the conditions of study.

Animals↗
PubMedDate not supplied

Haemodynamic effects of a combination of propranolol and clonidine in patients with post-hepatitic cirrhosis.

The haemodynamic effects of a combination of propranolol and clonidine were evaluated in 20 patients with post-hepatitic cirrhosis. Haemodynamic measurements were taken before and 30 min after an intravenous injection of 0.1 mg/kg of propranolol. Thereafter, each patient was given an oral dose of 150 micrograms of clonidine and re-measured 60 min later. In this series, eight patients were defined as 'non-responders' (a decrease in hepatic venous pressure gradient of < 10%) after propranolol treatment. Of both the responders and non-responders, propranolol caused expected decreases in the cardiac index and heart rate while mean arterial pressure remained unchanged. Of the propranolol responders, a significant decrease in hepatic venous pressure gradient was observed. After the addition of clonidine, in both the responders and non-responders there was a further decrease in hepatic venous pressure gradient with a concurrent drop in mean arterial pressure, but cardiac index and heart rate remained unaltered. In conclusion, the combination of propranolol and clonidine in post-hepatitic cirrhotic patients enhanced the reduction of portal pressure achieved by propranolol alone. The beneficial effects of the combination of the two in the reduction of portal pressure appeared to be similar in both the propranolol responders and non-responders. However, the drop in mean arterial pressure following the addition of clonidine may be hazardous to cirrhotic patients.

Adrenergic alpha-Agonists↗
PubMed1996

Haemodynamic effects of combined treatment with molsidomine and propranolol on portal hypertension in conscious and unrestrained cirrhotic rats.

We investigated the systemic and splanchnic haemodynamic effects of combined treatment with molsidomine and propranolol on cirrhotic rats. Liver cirrhosis was produced by repeated intraperitoneal injections of thioacetamide. The blood flow of each organ was measured serially using the radioactive microsphere method in the awake state before and after the administration of each agent. Cirrhotic rats received molsidomine (0-.5 mg/kg), propranolol (0.1 or 0.2 mg/min), both agents or placebo. Combination treatment with molsidomine and 0.1 mg/min propranolol significantly reduced portal pressure compared with molsidomine or propranolol alone (21 +/- 4 vs 15 +/- 3 or 11 +/- 2% P < 0.05). Systemic haemodynamic changes with this combined treatment were mild. This combined treatment slightly inhibited the molsidomine-induced decrease in portal vascular resistance (27 +/- 9 vs 31 +/- 6; NS) and markedly inhibited the molsidomine-induced decrease in splanchnic arterial resistance (7 +/- 6 vs 27 +/- 5% P < 0.05). Compared with low-dose propranolol administration, the combined treatment was associated with a significant decrease in portal vascular resistance (27 +/- 9% decrease vs 2 +/- 2% increase; P < 0.001) and a significant decrease in splanchnic arterial resistance (7 +/- 6% decrease vs 5 +/- 4% increase P < 0.05). The combination of molsidomine and high-dose propranolol (0.2 mg/min) caused a marked reduction in portal venous inflow, mean arterial pressure and cardiac index. We conclude that propranolol enhances the molsidomine-induced decrease in portal pressure by splanchnic vasoconstriction in association with a slight decrease in portal vascular resistance. The combination therapy with molsidomine and low-dose propranolol combination had more beneficial and less harmful effects on systemic and splanchnic haemodynamics and thus appears to be a superior method for treating portal hypertension.

Animals↗
PubMed1987

Effects of propranolol and swim-training on blood pressure, plasma electrolytes, and vasopressin in spontaneously hypertensive and normotensive rats.

The aim of this work was to study the influence of beta-adrenoreceptor blockade on the adaptation to exercise of one of the hormonal systems (arginine vasopressin) involved in the regulation of blood volume and pressure in spontaneously hypertensive rats (SHR). Systolic blood pressure (SBP) was measured in SHR and WKY rats during 11 wk of swim training. At the end of the training program we determined post-exercise values of plasma arginine-vasopressin (pAVP), osmolality (pOsm), K+ (pK+), Na+ (pNa+), hemoglobin (Hgb), and hematocrit (Hct) in SHR and WKY rats. The following groups were studied: control (C), propranolol treated (PC), swim trained (S), and propranolol-treated and swim-treated (PS). SBP was significantly reduced by swim training or propranolol, bu these beneficial effects on SBP were attenuated when propranolol and swim training were combined. pNa+ and pOsm were significantly reduced by training alone in SHR. This reduction of pNa+ and, consequently, of pOsmol without any modification of other parameters could suggest an Na+ loss. In contrast, the SHR group treated with propranolol alone showed a significant reduction in Hct, suggesting an increased plasma volume without Na+ loss. PS SHR showed a significant reduction of Hgb, Hct, proteins, pNa+, and pOsmol, probably as a consequence of the additive effects of swimming- and propranolol-induced hypervolemia with Na+ loss. The slight and nonsignificant reduction in pAVP observed with either training or propranolol treatment alone became much more pronounced and statistically significant when the 2 treatments were combined. WKY rats showed a much smaller response to exercise and beta-adrenoreceptor blockade than SHR. We conclude that the hypervolemia suggested in PS SHR could be a possible cause of attenuation of the beneficial effects of either swimming or propranolol on SBP.

Animals↗
PubMed1968

A comparison of some cardiovascular properties of propranolol, MJ 1999 and quinidine in relation to their effects in hypertensive animals.

1. A comparison of some cardiovascular effects of propranolol, MJ 1999 and quinidine has been made in rats and dogs.2. After intravenous, subcutaneous or oral administration to rats and dogs, propranolol was found to be 2-4 times more potent than MJ 1999 in blocking the chronotropic and vasodepressor responses to intravenously administered isoprenaline.3. Propranolol and quinidine affected the e.c.g. of rats and dogs in a similar manner.4. At dose-levels causing effective blockade of beta-receptors propranolol and MJ 1999 had no hypotensive effect after short- or long-term administration to conscious hypertensive rats and dogs.5. At very high dose-levels propranolol and quinidine, but not MJ 1999, lowered blood pressure in the hypertensive rat. This effect of propranolol is probably related to one or more of the properties that propranolol and quinidine have in common rather than to a blockade of beta-receptors.6. The possible relevance of these results to the use of propranolol as a hypotensive agent in man is discussed.

Anilides↗
PubMed1969

Inhibition of the carotid sinus reflex by the chronic administration of propranolol.

1. The changes in heart rate and arterial pressure produced by the intravenous injection of isoprenaline (0.5 mug/kg), noradrenaline (1.0 mug/kg), phenylethylamine (0.5 mg/kg), amphetamine (0.5 mg/kg) and by bilateral occlusion of the carotid arteries and by stimulation of the central ends of both vagus nerves have been recorded in groups of dogs anaesthetized with pentobarbitone.2. The acute intravenous injection of propranolol (1 mg/kg) reduced the increases in heart rate produced by the six procedures, the increases in arterial pressure in response to the last five procedures and the decrease in pressure produced by isoprenaline.3. This decrease produced by propranolol in the pressor responses resulted from a reduction in the increases in cardiac output elicited by the five procedures and has been attributed to blockade of cardiac adrenergic beta-receptors.4. Three groups of dogs were pretreated for 6 weeks by the oral administration of either placebo, propranolol 50 mg/kg daily or propranolol 10 mg/kg twice daily. The responses to the six test procedures were obtained 17-24 hr after the last dose of propranolol, when only minimal blockade of adrenergic beta-receptors was present. In the propranolol-treated groups, the pressor response to carotid occlusion but not to the other test procedures was significantly reduced.5. The pressor response to carotid occlusion was not reduced in a fourth group of dogs given a single dose of propranolol (50 mg/kg) 24 hr before the test procedures.6. The mechanism of this selective reduction in the pressor response to occlusion of the carotid arteries is not clear. It is suggested that it may contribute to the hypotensive action of propranolol in man during prolonged oral administration.

Amphetamine↗