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PubMedDate not supplied

Induction of propranolol metabolism in isolated rats hepatocytes treated by di(2-ethylhexyl) phthalate (DEHP) and mono(2-ethylhexyl) phthalate (MEHP).

Blood lines of polyvinyl chloride (PVC) for hemodialysis usually contain di(2-ethylhexyl) phthalate (DEHP) as a plasticizer. Previous studies show that 1 mg/kg of this plasticizer can leach into the blood during one dialysis session. It is rapidly metabolized in the liver. Mono(2-ehtylhexyl) phthalate (MEHP), its main metabolite can be detected as well. After oral administration to rodents, both compounds caused a variety of adverse biological effects such as testicular atrophy, peroxisome proliferation and hepatic peroxisomal enzyme induction. Male wistar rats were treated intraperitoneally by DEHP and MEHP using twice the dose of that involved in human exposure during a dialysis session. Propranolol metabolism by hepatocytes was investigated after fresh isolation from treated and untreated rats by means of reverse phase HPLC. The choice of propranolol as a substrate was made because of its rather quick liver metabolisation. Phenobarbital was chosen in the study as a reference of enzymatic inducer to evaluate the inducing effect of DEHP and MEHP. Propranolol was metabolized by the hepatocytes of both treated and untreated rats. Hepatocytes isolated from rats treated by phenobarbital, MEHP and DEHP were shown to have a higher speed constant of metabolism indicating a rapid metabolism of propranolol. Under these conditions, in fact, propranolol metabolisation was found to be respectively 6, 2.7, 2 times faster than the propranolol metabolisation of untreated rats. The hypothesis that DEHP and MEHP are enzymatic inducers, particularly cytochrome P450 (CYP) inducers of the xenobiotics metabolism on the intact liver after IP administration has become been found to be valid. The results obtained in this study confirm the value of isolated hepatocytes as an in vivo drug metabolism predictive model.

Animals↗
PubMedDate not supplied

Effect of propranolol on aldosterone response to heat exposure in sodium-restricted men.

To assess the role of the renin-angiotensin system in the control of aldosterone reease in response to heat exposure, 6 sodium restricted subjects were studied on three random experimental days: a control day and two heat exposure days (46C, 35 mbar, 90 min) with and without propranolol. Plasma aldosterone, renin activity, ACTH and K+ were determined from plasma samples taken every 20 min from 08:00 to 14:00. After propranolol administration, plasma aldosterone responsiveness to heat exposure increased, though plasma renin activity was depressed. Concurrently, propranolol reduced heat tolerance, leading to an increased ACTH and cortisol release in 3 of the subjects. Plasma levels of K+ were not significantly different during both heat exposure days. The enhanced response of plasma aldosterone may in part be related to the concurrent rises in ACTH, but a similar sustained aldosterone response was observed in subjects without ACTH release. Except for a significantly lower heart rate, propranolol induced no changes in hemodynamic and thermal response to heat. Plasma volume, blood pressure, sodium excretion, mean skin and rectal temperature rises and body weight losses were not modified by prior administration of the drug. The dissociation between aldosterone and renin activity after propranolol administration suggests that the aldosterone response to heat exposure is not primarily mediated by changes in activity of the renin-angiotensin system. Propranolol may lead to a reduced metabolic clearance rate of aldosterone or increase the sensitivity of the adrenal cortex to concomitant changes in the known stimuli, but the involvement of an additional factor in aldosterone regulation during heat exposure cannot be excluded.

Adrenocorticotropic Hormone↗
PubMed1997

Propranolol-induced seizures in mice: the role of noradrenaline.

The effects of some noradrenergic agents, phenobarbitone, diazepam and phenytoin on seizures produced by propranolol were investigated in mice. Isoprenaline and DL-threo-3,4-dihydroxyphenylserine (DOPS) effectively antagonized the seizures elicited by propranolol. Pargyline and imipramine significantly attenuated propranolol-induced seizures and also significantly potentiated the protecting effect of DOPS against the seizures. alpha-Methyl-p-tyrosine, disulfiram and reserpine significantly potentiated propranolol-elicited seizures. However, DOPS significantly antagonized the seizure-potentiating effects of alpha-methyl-p-tyrosine, disulfiram and reserpine. Phenylephrine, clonidine, prazosin, idazoxan, phenobarbitone, diazepam and phenytoin did not significantly alter propranolol-induced seizures. These results suggest that propranolol-induced seizures in mice may involve a noradrenergic mechanism mediated via central beta-adrenoceptors.

Adrenergic Uptake Inhibitors↗
PubMed2000

Pharmacokinetics of propranolol and atenolol in patients after partial gastric resection: a comparative study.

OBJECTIVE: Partial gastric resection alters the anatomy and secretory activity of the gastrointestinal tract. It might be expected that the consequences of such changes should affect the pharmacokinetics, especially concerning the absorption of orally administered drugs. Propranolol and atenolol, as representatives of lipophilic and hydrophilic beta-adrenoreceptor antagonists, have been studied in order to define their pharmacokinetic characteristics in patients after partial gastrectomy. METHODS: The study was carried out in 29 patients after gastric resection with Billroth I (B1) anastomosis and in 18 healthy volunteers as controls. Pharmacokinetics of propranolol and atenolol was investigated after a single oral dose of 80 mg and 100 mg, respectively, following a cross-over schedule. Blood samples were collected ten times during the 24 h after the drug administration. Pharmacokinetic parameters of propranolol and atenolol were calculated using a one-compartment open model with first-order absorption. RESULTS: The average blood plasma concentrations of propranolol in gastrectomised patients were lower than those in controls, reaching significance between 1.5 h and 6.0 h of the observation period. Pharmacokinetic parameters of propranolol were different in subjects submitted to surgery compared with healthy persons. We observed a significant decrease in the area under the concentration-time curve (32%) and the peak plasma concentration (20%), and an increase in half-life (25%). Mean plasma concentrations and pharmacokinetic parameters of atenolol in patients following partial gastric resection were not significantly different from those in the controls. No relationship between time interval following partial gastrectomy and pharmacokinetic parameters of the investigated drugs was noted. CONCLUSION: Partial gastrectomy with B1 anastomosis affects the pharmacokinetics of propranolol (lipophilic drug) but not atenolol (hydrophilic drug).

Adrenergic beta-Antagonists↗
PubMed1979

Contrasting effects of acute beta blockade with propranolol on plasma catecholamines and renin in essential hypertension: a possible basis for the delayed antihypertensive response.

Blood pressure, heart rate, plasma renin activity, plasma norepinephrine and plasma epinephrine were determined in 11 patients with essential hypertension at rest before and 15, 30, 45, and 60 minutes after an intravenous infusion of 0.12 mg./Kg. propranolol given over five minutes. After propranolol mean blood pressure was unchanged; heart rate decreased by 14 per cent within 15 minutes and showed no further changes. Plasma renin activity decreased progressively by 48 per cent 60 minutes after propranolol, whereas plasma norepinephrine and epinephrine were always higher after propranolol than control values. Increases in norepinephrine were statistically significant at 30, 45, and 60 minutes (respectively 49, 39, and 45 per cent, P less than 0.005 at least) and those of epinephrine even at 15 minutes (respectively 60, 82, 62, and 94 per cent P less than 0.01 for all). These results indicate that acute beta blockade with propranolol incudes increases in circulating plasma norepinephrine and epinephrine which might be consequent to rapidly induced hemodynamic changes. This augmented sympathetic activity might explain why propranolol, when acutely infused, does not decrease blood pressure despite effective cardiac and renin blockade.

Adrenergic beta-Antagonists↗
PubMed1983

Double-blind randomized crossover trial of verapamil and propranolol in chronic stable angina.

Propranolol (240 mg daily) and verapamil (360 mg daily) were objectively compared for their respective efficacy in the treatment of chronic stable angina pectoris. Twenty-two patients were studied in a randomized placebo controlled, double-blind crossover trial with 4 weeks on each active drug treatment. Multistage treadmill exercise with computer-assisted ECG analysis was performed after 2 weeks on placebo and at the end of each 4-week active drug treatment. The mean exercise time to produce angina was 5.5 minutes (SEM +/- 0.4 minutes) on placebo and this increased to 7.8 (+/- 0.5) minutes on propranolol and 9.1 (+/- 0.5) minutes on verapamil. The improvement in exercise time of verapamil over propranolol was statistically significant (p less than 0.01). Ten patients became free of angina with verapamil and four with propranolol. Resting and maximal exercise heart rates were significantly reduced by propranolol; verapamil did not reduce the maximal heart rate but reduced the resting heart rate slightly. However, the heart rate increase per minute of exercise was significantly diminished (p less than 0.001). ST segment changes showed improvement with both drugs despite marked differences in heart rate profile. The overall efficacy of the slow calcium channel blocker, verapamil, compares favorably with that of a standard beta-adrenoreceptor blocking drug (propranolol), thus providing a new perspective in the management of angina pectoris. These two classes of drugs seem to act by different mechanisms and it is suggested that if patients are resistant or intolerant to one of these drugs, the other can be used to yield a beneficial response.

Adult↗
PubMed1983

Effect of a twelve-hour hiatus in propranolol therapy on exercise tolerance in patients with angina pectoris.

To determine whether propranolol can be administered twice daily without any loss of antianginal effect, we studied nine men receiving long-term propranolol therapy for stable angina pectoris. Each patient performed bicycle exercise to the point of angina on two consecutive mornings. By means of double-blind placebo-propranolol administration before the test, the study created a situation whereby on one day the exercise took place 12 hours after the last dose of propranolol, and on the other day 1 1/2 hours after a dose. Despite markedly lower blood levels of propranolol on the day that exercise was performed 12 hours after the last dose, exercise time to angina was nearly identical on the 2 days. We conclude that long-term therapy with propranolol for angina pectoris can be administered on a twice daily basis with no loss of effectiveness.

Adult↗
PubMed1984

Comparative effects of propranolol and nadolol on renal blood flow in normal rats and rats with congestive heart failure.

Mean arterial blood pressure (MAP), heart rate (HR), renal blood flow (RBF), and renal vascular resistance (RVR) were determined before and during an infusion of propranolol (18 mg/kg/hr) or nadolol (30 mg/kg/hr) in anesthetized Munich-Wistar rats with normal cardiac function. Eight rats treated with propranolol had significant reductions in MAP (110 to 98 mm Hg; p less than 0.05) and HR (316 to 242 bpm; p less than 0.01), accompanied by a 24% decrease in RBF (5.9 to 4.5 ml/min; p less than 0.05) and a 22% increase in RVR (19.4 to 23.7 mm Hg/ml/min; p less than 0.05). Although nadolol also reduced MAP (104 to 93 mm Hg; p less than 0.01) and HR (315 to 268 bpm; p less than 0.05) in eight other rats, RBF and RVR remained unchanged from baseline levels. Thus, despite similar decrements in MAP and HR, propranolol decreased renal perfusion, whereas nadolol maintained it in animals with noninfarcted myocardium. These parameters were also evaluated in rats with congestive heart failure induced by myocardial infarction at least 3 weeks prior to their receiving either propranolol (18 mg/kg/hr; n = 6) or nadolol (30 mg/kg/hr; n = 6). In the basal state, rats with congestive heart failure had significantly (p less than 0.05) lower MAP, HR, and RBF and higher (p less than 0.01) RVR compared with control rats. Propranolol and nadolol induced comparable falls (p less than 0.05) in MAP and HR. Whereas RBF tended to fall with propranolol (3.3 to 2.4 ml/min), renal perfusion was well maintained with nadolol (3.4 to 3.8 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1984

A comparison of propranolol and nadolol pharmacokinetics and clinical effects in thyrotoxicosis.

For a comparison of propranolol and nadolol pharmacokinetics and clinical effects, 20 newly diagnosed patients with thyrotoxicosis were randomly selected to receive as sole therapy, either propranolol, 40 mg every 6 hours for 14 days, or nadolol, 80 mg each morning for 14 days. The study was repeated when the patients were in the euthyroid state. There was a similar and highly significant degree of beta blockade and amelioration of symptoms of thyrotoxicosis at the end of the dosage interval (trough), i.e., 24 hours after nadolol or 6 to 8 hours after propranolol. Trough and peak serum levels of propranolol were significantly lower when the patients were in a thyrotoxic state than when they were in a euthyroid state, whereas the pharmacokinetics of nadolol were not appreciably altered by thyrotoxicosis. In thyrotoxicosis, trough levels of propranolol and nadolol were significantly inversely correlated with derived creatinine clearance values. In the symptomatic treatment of thyrotoxicosis, nadolol, a once-daily nonmetabolized beta blocker, has certain advantages compared with propranolol. It is preferred by patients, is more convenient, and probably aids compliance.

Adolescent↗
PubMed1985

Propranolol-induced changes in ventricular isomyosin composition in the rat.

The ventricular isomyosin composition in the rat is characterized by three isoenzymes, V1, V2, and V3, with high, intermediate, and low Ca++-activated ATPase activity, speed of muscle shortening, and contractile economy. In this study, we examined the effects of propranolol on ventricular isomyosin composition in the rat. Eight 4-week-old male Wistar rats were treated from 4 to 12 weeks of age with daily 10 mg/kg subcutaneous doses of propranolol; four control rats were given subcutaneous distilled water. At the end of the treatment period, the efficacy of beta blockade was confirmed by isoproterenol test in some rats from each group. After the rats were killed left ventricular myosin from both control and propranolol-treated animals was purified and tested for Ca++-activated ATPase activity. Ventricular isomyosin composition was studied by gel electrophoresis in non-denaturing conditions. Heart rate was significantly lower in the propranolol group, while no differences in blood pressure, body weight, or ventricular weight were found between the two groups. Lower Ca++-activated ATPase activity values and a higher expression of myosin isoenzymes V2 and V3 were found in propranolol-treated rats. Possible links between the observed shift in ventricular isomyosin composition and the well-known modifications in myocardial contractility and oxygen consumption occurring after chronic propranolol administration remain to be established.

Animals↗
PubMed1986

Effects of propranolol on myocardial damage resulting from coronary artery occlusion followed by reperfusion.

To evaluate the effects of propranolol on myocardial metabolism after coronary reperfusion, serial measurements of myocardial creatine kinase (CK) and calcium (Ca) contents and CK and lactic acid (LA) concentrations in coronary sinus blood were carried out in 33 open-chest dogs. The left anterior descending coronary artery was occluded for 60 minutes and was then reopened. Twelve of the dogs were given propranolol before occlusion. Reperfusion for 30 minutes in dogs with and without propranolol pretreatment resulted in reduced myocardial CK in the ischemic region and rapidly elevated plasma CK and LA. However, when compared with the control group, the propranolol-treated group showed smaller changes in myocardial CK and plasma LA. Myocardial Ca in the ischemic region was significantly higher than that in the nonischemic region in the control group, but not in the propranolol-treated group. It was concluded that propranolol was protective against myocardial damage resulting from coronary occlusion followed by reperfusion.

Animals↗
PubMed1988

Differential sensitivity of sinus node, atrioventricular node, atrium, and ventricle to propranolol.

The purpose of this study was to test the hypothesis that less propranolol was required to block stellate-induced shortening of atrial and ventricular effective refractory periods (ERPs) than was required to prevent stellate-induced shortening of the spontaneous sinus nodal cycle length and atrioventricular (AV) nodal conduction time. Studies were performed in open-chest, neurally decentralized dogs anesthetized with secobarbital. We determined the dose of propranolol (propranolol dose-response curves) required to block the effects of 1 Hz, 2 Hz, and 4 Hz bilateral ansae subclaviae stimulation on sinus nodal automaticity, AV nodal conduction, and atrial and ventricular ERPs. We found that propranolol at a dose of 0.5 mg/kg eliminated ansae subclaviae-induced shortening of atrial and ventricular ERPs, whereas sinus nodal cycle length and AV nodal conduction time still shortened. These data indicate a differential sensitivity of the sinus and AV nodes compared with atrial and ventricular myocardium to the beta-adrenergic receptor-blocking effects of propranolol in response to efferent sympathetic neural stimulation. Clinical implications are that it might be possible to treat sympathetically mediated ventricular arrhythmias with doses of propranolol that still preserve sinus and AV nodal responses.

Animals↗
PubMed1976

Long-term propranolol therapy for angina pectoris.

Sixty-three patients with stable, severe typical angina pectoris (New York Heart Association functional class III or IV) were treated with propranolol and studied prospectively with a follow-up period of 5 to 8 years to assess the rate of complications and long-term effectiveness after an initial control period. The patients' mean age was 56 years; the mean daily dose of propranolol was 255 mg. The average yearly mortality rate was 3.8 percent with a cumulative 5 year mortality rate of 19 percent. Patients whose reduction of angina with propranolol was less than 50 percent had a nearly four-fold greater mortality rate than those whose reduction was 50 percent or more (P less than 0.01). Thirty-two percent of patients per year were angina-free with propranolol and 84 percent per year had 50 percent or more reduction in anginal episodes. There was no evidence for tachyphylaxis. Heart failure developed in 25 percent of patients, two thirds of whom had either congestive heart failure with an acute infarction or a prior history of congestive heart failure. All patients whose initial cardiothoracic ratio was greater than 0.5 had heart failure during the first 3 years of propranolol therapy. Of 12 patients who had an acute infarction during therapy, 7 died, 6 with cardiogenic shock; in contrast, 8 of 9 patients who had congestive heart failure without acute infarction survived. Eight percent of patients had other significant side effects, including gastrointestinal symptoms (three patients), hallucinations (one) and postural hypotension (one). The occurrence of asthma in three patients was dose-related and did not require drug discontinuation. Propanolol is an effective form of long-term therapy for severe angina pectoris; it does not induce tachyphylaxis or increase the overall mortality rate, although it may increase the risk of cardiogenic shock in acute myocardial infarction. Previous history of congestive heart failure, a cardiothoracic ratio of more than 0.5 without overt heart failure and mild asthma are relative contraindications. A 50 percent or greater reduction in anginal pain with propranolol predicts a low mortality group.

Adult↗
PubMed1976

Propranolol therapy in patients undergoing myocardial revascularization.

The records of 185 consecutive patients having myocardial revascularization were reviewed with regard to preoperative administration of propranolol and intraoperative or postoperative complications. Tachycardia and hypertension before cardiopulmonary bypass were slightly more common in patients never taking propranolol or those who had discontinued it for more than 48 hours before operation. There was no statistically significant difference in the incidence of postbypass hypotension among patients who took propranolol within 24 hours of operation, those who discontinued it more than 24 hours before operation, and those who never took the drug. Operative mortality was not significantly different among patients who received propranolol within 48 hours of operation (3%), those who never took it and those who discontinued it more than 48 hours before operation (4%). Early in the series, five patients had an acute myocardial infarction within 48 hours after routine preoperative withdrawal of propranolol. Because complete withdrawal of propranolol in patients with unstable angina pectoris may lead to acute myocardial infarction, we recommend gradual withdrawal of the drug during 48 hours before operation. If this is not possible because anginal pain recurs or intensifies, then reduced doses may be given safely up to 10 hours before revascularization, provided that the patient is a satisfactory candidate for bypass and that adequate myocardial revascularization can be accomplished.

Adult↗
PubMed1978

Propranolol rebound--a retrospective study.

To assess the effects of sudden withdrawal of propranolol on inpatients with coronary artery disease, 102 patients admitted for cardiac catheterization were evaluated. Criteria for inclusion in the study were angiographically documented coronary artery disease, propranolol therapy at a mean daily dose of at least 80 mg and abrupt discontinuation of propranolol therapy before catheterization. There were 55 patients (mean age 52.5) who discontinued propranolol therapy (mean daily dose 127 mg) and a control group of 47 patients (mean age 53) who continued to receive propranolol (mean daily dose 143 mg). The criteria for morbidity were death, myocardial infarction or change in pain pattern. In the withdrawal group there were no deaths, one myocardial infarction judged to be related to catheterization and only one instance of a change in pain pattern. Thus, propranolol rebound appears to occur infrequently among hospitalized patients with reduced activity.

Adult↗
PubMed1981

Effect of propranolol on postexercise left ventricular ejection time index.

The net delta left ventricular ejection time index 4 minutes after exercise is prolonged in many patients with coronary artery disease. This prolongation is thought to be due to the lack of response of the ischemic myocardium to adrenergic stimulation and has been proposed as a measure of myocardial ischemia. In this study, the effect of beta adrenergic blockade on net delta left ventricular ejection time was studied in nine normal subjects (Group A) and in eight patients with stable angina and coronary artery disease (Group B). In Group A, a treadmill exercise test was performed for 10 minutes before and after administration of propranolol, 160 mg daily, for 2 days. The postexercise net delta left ventricular ejection time was significantly greater after propranolol (mean +/- standard error of the mean 12 +/- 4 versus 35 +/- 4 ms, p less than 0.01). In group B a maximal treadmill exercise test was performed before and after therapy with propranolol. Only patients with a normal net delta left ventricular ejection time before propranolol were selected. The net delta left ventricular ejection time again increased significantly after propranolol (11.5 +/- 4 versus 35.3 +/- 5 ms p less than 0.01). It is concluded that prolongation of postexercise net delta left ventricular ejection time cannot be used to diagnose ischemia in patients who are receiving propranolol therapy. Our data support the hypothesis that prolongation of net delta left ventricular ejection time after exercise is caused by an impaired myocardial response to catecholamines, whether due to ischemia or effective beta adrenergic blockade.

Adult↗
PubMed1982

Combined therapy with verapamil and propranolol in chronic stable angina.

The comparative efficacy of verapamil (360 mg daily) and propranolol (240 mg daily) was evaluated with computerized treadmill exercise in 22 patients with chronic stable angina in a placebo-controlled double-blind crossover study with 4 weeks on each active phase. Fourteen of these patients still had angina despite active drug therapy and they were further treated with a combination of verapamil (360 mg) and propranolol (120 mg) for 4 weeks. The mean exercise time for these patients taking placebo was 4.8 +/- 0.22 minutes (mean +/- standard error of the mean) and this increased to 6.8 +/- 0.64 minutes with propranolol and 8.0 +/- 0.5 minutes with verapamil. A further increase to 10.1 +/- 0.88 minutes was observed with the combination of both drugs and seven patients became symptom-free. S-T segment criteria improved with both drugs, and combination therapy produced a further reduction in peak S-T depression. Electrocardiographic ambulatory monitoring showed no evidence of conduction defects and mean hourly heart rates were similar to those seen with propranolol alone. Left ventricular function indexes were not significantly different from those obtained with propranolol. Combination therapy with verapamil and propranolol appears to be efficacious in the treatment of selected patients with severe chronic stable angina. The patients need to be carefully monitored for adverse effects.

Adult↗
PubMed1982

Reversal of regional myocardial depressant effects of propranolol with nitroglycerin.

Use of propranolol in acute myocardial infarction is limited by its cardiodepressant effects. The effects of nitroglycerin (0.4 mg intravenously) on regional myocardial dysfunction produced by total or partial (50 percent) coronary occlusion and intravenous administration of propranolol (1.0 mg/kg) were evaluated using pairs of ultrasonic crystals implanted subendocardially in the nonischemic and ischemic zones in 14 open chest dogs. During partial coronary occlusion, systolic shortening (% delta L) in the ischemic zone decreased from 20.9 +/- 5.3 to 7.2 +/- 6.4 (p less than 0.001). Propranolol did not change it significantly. Nitroglycerin increased % delta L from 6.7 +/- 4.5 to 11.2 +/- 5.3 (p less than 0.01). The nonischemic zone was unaffected by partial coronary occlusion but showed a decrease in % delta L from 18.6 +/- 6.2 to 15.6 +/- 5.1 (p less than 0.01) with propranolol. Nitroglycerin increased % delta L from 15.6 +/- 5.1 to 17.3 +/- 5.9 (p less than 0.02). During total coronary occlusion, nitroglycerin administration after propranolol improved % delta L in the nonischemic but not in the ischemic zone. Nitroglycerin caused a significant decrease in left ventricular systolic and end-diastolic pressures. Heart rate remained unchanged. It is concluded that nitroglycerin reversed myocardial depressant effects of propranolol in both the partially ischemic and the nonischemic zones after acute coronary occlusion.

Animals↗