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PubMed1989

Improvement in functional recovery of stunned canine myocardium by long-term pretreatment with oral propranolol.

We investigated the effect of long-term oral pretreatment with the beta-adrenergic antagonist, propranolol (Inderal LA, 160 mg daily for 8 days) on the functional recovery of myocardium after 15-minute coronary artery occlusion followed by 3 hours of reperfusion in barbital-anesthetized dogs. Propranolol-pretreated dogs (N = 9) displayed a significantly lower left ventricular peak-positive rise in ventricular pressure (dP/dt), heart rate, and rate-pressure product throughout the experiment compared with the control group (N = 15). Subendocardial percent segment shortening as measured by sonomicrometry recovered to 65.4 +/- 7.2% of the preocclusion level after pretreatment with propranolol, whereas the control group recovered to only 11.1% +/- 10.2% after 3 hours of reperfusion. To ascertain the beneficial role of a lower heart rate on the recovery of regional contractile function, a third group of dogs (N = 6) was pretreated with propranolol, but heart rate was maintained at control levels by atrial pacing. The beneficial effects of pretreatment with propranolol were abolished in this group. There were no differences between groups in myocardial perfusion in the normal region as measured by the radioactive microsphere technique. However, in postischemic, reperfused myocardium, there was a significantly higher blood flow to subepicardium, mid-myocardium, and subendocardium after reperfusion in the propranolol-pretreated, unpaced group. Thus long-term oral pretreatment with propranolol enhances the contractile recovery of postischemic, reperfused myocardium. This protective effect of beta-adrenergic blockade is primarily related to the reduction in heart rate and enhanced perfusion in the postischemic region.

Administration, Oral↗
PubMed1991

Propranolol therapy alters estimation of potential cardiovascular risk derived from submaximal postinfarction exercise testing.

We studied the effect of propranolol administration on risk assessment based on submaximal exercise testing performed early after myocardial infarction. A total of 70 patients with recent infarction underwent modified Bruce treadmill testing with simultaneous measurement of expired gases in the absence of antianginal agents including beta-antagonists. Among these, 31 patients who had at least one of the following abnormalities--ST depression greater than or equal to 1 mm (22 patients), chest pain (four patients), or treadmill time less than 360 seconds (12 patients)--were studied in a randomized double-blind fashion and received either placebo or 240 mg of propranolol/day. A total of 28 patients completed the randomized phase and were able to undergo repeat exercise testing an average of 3.4 +/- 1.8 days later. Randomized groups were equivalent at baseline except for a higher peak oxygen consumption and carbon dioxide production (p less than 0.05) in the propranolol compared with the placebo group; these differences were taken into account in statistical analyses of the study data. Resting heart rate (59 +/- 1.2 versus 82 +/- 4.2 beats/min) and peak heart rate x systolic blood pressure (14,208 +/- 496 versus 20,075 +/- 1,062) were both significantly less (p less than 0.01) after propranolol than after placebo. Eight of nine patients treated with placebo maintained ST depression greater than or equal to 1 mm from the initial to the randomized exercise test, compared with only 4 of 13 receiving propranolol (p less than 0.01). In those with continued ST depression, time to positivity was significantly longer in those receiving propranolol compared with those taking placebo (538 +/- 73 versus 318 +/- 44 seconds, p less than 0.05). In contrast, the peak ratio between carbon dioxide production and oxygen consumption was higher in those receiving propranolol compared with those receiving placebo (0.93 +/- 0.04 versus 0.81 +/- 0.03, p less than 0.05). We conclude that propranolol therapy reduces evidence of ischemia and changes traditional estimates of potential cardiac risk derived from submaximal postinfarction exercise testing.

Cardiovascular Diseases↗
PubMed1977

Altered hemoglobin-oxygen affinity with long-term propranolol therapy in patients with coronary artery disease.

Pharmacologic agents that alter hemoglobin affinity for oxygen may affect systemic or myocardial oxygen delivery. In vitro, and in normal man propranolol shifts the oxyhemoglobin equilibrium curve to the right, thus increasing the partial pressure of oxygen at which hemoglobin is 50% saturated (P50) and enhancing oxygen delivery. The effect of propranolol on hemoglobin P50 was evaluated in 12 patients with angina pectoris and documented coronary artery disease. Determinations were made during oral propranolol therapy (mean daily dose 152 mg) of at least 3 months' duration and after administration of propranolol had been discontinued for at least 4 days. Hemoglobin P50 and erythrocyte 2,3-diphosphoglycerate (DPG) were measured. Data in 12 patients were: the mean P50 after discontinuation of propranolol was 28.2 mm Hg+/-0.9 (standard error of the mean) and during propranolol therapy 31.7+/-0.7; P less than 0.001; red blood cell 2,3-DPG did not change to explain the increase in P50. This demonstrated shift could increase systemic oxygen delivery and thus benefit marginally perfused myocardium while sparing coronary flow. Propranolol, in addition to its negative chronotropic and inotropic effects, may increase tissue oxygen delivery in patients with the anginal syndrome.

Coronary Disease↗
PubMed1977

Blood pressure, renin activity and heart rate changes during propranolol therapy of hypertension.

To investigate the importance of plasma renin activity in determining the antihypertensive action of propranolol and of heart rate in guiding propranolol therapy, the effect of a graded oral dose of propranolol on blood pressure, plasma renin and heart rate was studied in 24 men with essential hypertension and differing initial levels of renin activity. Although plasma renin decreased substantially in patients with normal and high renin levels tasking a small dose of propranolol (40 mg/day), blood pressure was unchanged in the normal renin group, and a small decrease in systolic pressure alone was noted in those with high plasma levels of renin. Patients with low renin levels had no reduction in blood pressure with small doses of propranolol, but as a group they responded well to a dose of 320 mg/day. Standing heart rate decreased maximally at plasma propranolol concentrations greater than 25 ng/ml, and did not exceed 72 beats/min with plasma concentrations above that level. Overall, the observed responses for plasma renin and heart were more pronounced at lower plasma propranolol concentrations than those for blood pressure.

Adult↗
PubMed1982

Comparison of oral propranolol and verapamil for combined systemic hypertension and angina pectoris. A placebo-controlled double-blind randomized crossover trial.

The relative efficacies of oral verapamil, a calcium-entry blocking drug, and propranolol, a beta-adrenergic blocking drug, were compared in 12 patients who had both stable angina pectoris and mild to moderate systemic hypertension, using a placebo-controlled, double-blind, randomized crossover protocol. Compared with placebo, both propranolol and verapamil decreased the frequency of anginal attacks and the number of nitroglycerin tablets consumed, and increased exercise duration and total work; there were no significant differences in the antianginal effect of the two drugs. Both verapamil and propranolol reduced the supine and standing systolic and diastolic blood pressure measured at rest; compared with propranolol, however, verapamil had greater effects on standing diastolic blood pressure (p less than 0.002). Resting heart rate was reduced from placebo baseline with large doses of both drugs; compared with verapamil, however, propranolol exerted greater effects on resting heart rate and rate-pressure product. Plasma renin activity was increased from placebo baseline with verapamil (p less than 0.05), but was reduced with propranolol (p less than 0.05); no significant change in plasma aldosterone was seen with either drug. Verapamil appears to be a safe and effective treatment alternative to propranolol for relieving anginal symptoms, improving exercise tolerance, and reducing elevated systemic blood pressure in patients with both angina pectoris and mild to moderate systemic hypertension.

Adrenergic beta-Antagonists↗
PubMed1982

Comparative effects of abrupt withdrawal of propranolol and verapamil in angina pectoris.

The potential hazards of abrupt withdrawal of propranolol have been described in patients with angina pectoris; however, the effects of abrupt withdrawal from long-term therapy with verapamil have not previously been investigated. The comparative effects of withdrawal from long-term treatment with propranolol and verapamil were assessed in a placebo-controlled double-blind randomized crossover study of 20 patients received placebo for 2 weeks, then increasing doses of propranolol (60 to 320 mg/day) or verapamil (240 to 480 mg/day) for 3 weeks. Patients were then abruptly withdrawn from drug onto placebo for 1 week, followed by crossover to the other drug treatment and a second withdrawal period. All 20 patients were withdrawn from verapamil without evidence of a rebound increase in frequency of anginal attacks, blood pressure, heart rate, or rate-pressure product and without a rebound deterioration in exercise tolerance. In contrast, with propranolol withdrawal, 2 patients (with the highest baseline angina attack rate) had a severe exacerbation of their anginal syndrome and could not undergo formal exercise testing; the other 18 patients were withdrawn from propranolol without incident. Plasma catecholamines were increased during exercise compared with rest during all treatments; however, the levels of catecholamines during exercise were significantly higher with propranolol than with verapamil and placebo (p less than 0.05). Levels of exercise catecholamines returned to placebo baseline values after withdrawal of propranolol.

Angina Pectoris↗
PubMed1983

Comparison of high-dose and medium-dose propranolol in the relief of exercise-induced myocardial ischemia.

The effects of medium-dose (160 mg/day) and high-dose (480 mg/day) oral propranolol were compared in 22 patients who had typical angina pectoris and objective evidence of myocardial ischemia during exercise. Left ventricular (LV) ejection fraction (EF) and wall motion score (WMS) (an index of regional LV dysfunction) were assessed by radionuclide angiography both at rest and during exercise to the pretreatment maximum work load. Functional class improved in 11 of the 22 patients during medium-dose propranolol therapy. Medium-dose propranolol reduced mean resting heart rate from 71 to 55 beats/min, exercise heart rate from 122 to 93 beats/min, and exercise systolic blood pressure from 183 to 162 mm Hg (p less than 0.001 for each). The incidences of exercise-induced chest pain and S-T segment depression were reduced from 19 to 9 patients (p less than 0.001), and from 20 to 10 patients (p = 0.002), respectively. Medium-dose propranolol had no effect on mean EF or WMS at rest, but improved function in ischemic regions during exercise; WMS decreased (p = 0.001), and mean exercise EF increased from 0.51 to 0.56 (p = 0.025). Compared with the medium dose, high-dose propranolol improved functional class in 3 additional patients, and further reduced mean resting heart rate (from 55 to 52 beats/min, p = 0.001) and mean exercise heart rate (from 93 to 86 beats/min, p = 0.001). Exercise-induced chest pain and S-T segment depression were abolished in a further 7 and 6 patients, respectively. Exercise EF and WMS improved further in several patients, but the changes were not statistically significant for the group (p = 0.095 and 0.082, respectively). Thus, in patients with coronary artery disease and exercise-induced ischemia, propranolol reduced heart rate and blood pressure and the incidence of exercise-induced chest pain, electrocardiographic changes, and ischemic LV dysfunction. Although most of these effects were seen with medium-dose propranolol, higher doses provided additional relief of chest pain and S-T segment depression, and further improved global and regional LV function in several patients.

Angina Pectoris↗
PubMed1983

Comparison of the antiarrhythmic effects of acebutolol and propranolol in the treatment of ventricular arrhythmias.

This study was designed to assess the relative antiarrhythmic activity of fixed doses of 2 beta-adrenergic blocking agents, propranolol and acebutolol, in a prospective double-blind crossover trial. Twenty-one patients who had at least 30 premature ventricular contractions (PVCs) per hour while receiving placebo were entered into the study. Ten patients were randomized to initially receive propranolol, 40 mg every 8 hours, and 11 were assigned to receive acebutolol, 300 mg every 8 hours. After 6 weeks of treatment, patients were weaned off medication for 1 week and then placed on placebo for 1 week. Eighteen patients were available and eligible for crossover to the alternative regimen for an additional 6 weeks. All 21 patients completed courses with propranolol and 17 completed courses with acebutolol. The mean number of PVCs per hour during placebo, propranolol and acebutolol treatment were 267, 87 and 119, respectively. Using paired t test statistics on observation differences, both propranolol and acebutolol significantly reduced the number of PVCs per hour compared with placebo, whereas similar analysis revealed no significant difference in the antiarrhythmic effect. However, with the current sample size the power of the test is too low for the latter conclusion to be stated with confidence. Side effects were mild and infrequent, requiring discontinuation of acebutolol in 2 patients and discontinuation of propranolol in 1. Thus, acebutolol is a safe and effective antiarrhythmic agent and compares favorably with propranolol.

Acebutolol↗
PubMed1984

Comparison of oral MK 421 and propranolol in mild to moderate essential hypertension and their effects on arterial and venous vessels of the forearm.

The efficacy of MK 421 and propranolol was compared in 48 patients with mild to moderate hypertension. Each patient was randomly assigned to receive 1 of the drugs for 12 weeks. Additionally, a subgroup of 28 patients underwent studies of forearm arterial and venous circulation by means of pulsed Doppler and mercury-in-silastic plethysmography. Both drugs reduced supine and standing blood pressure (BP) (p less than 0.001). Propranolol reduced heart rate (p less than 0.001), while MK 421 did not change it. Brachial artery diameter, blood velocity and flow increased after MK 421 (p less than 0.001), but were not changed after propranolol therapy. Forearm vascular resistance decreased after MK 421 (p less than 0.001) and after propranolol (p less than 0.05). Forearm venous tone was unaffected on MK 421, but increased after propranolol (p less than 0.01). Thus, in moderate hypertension, 3 months of treatment with MK 421 or propranolol similarly decrease BP, but affect the forearm circulation differently: MK 421 dilates both the brachial artery and the arterioles of the forearm, but does not affect the venous vessels, and propranolol causes little arterial change but increases the forearm venous tone.

Adult↗
PubMed1984

Randomized, placebo-controlled evaluation of lidoflazine in patients receiving beta-blocker therapy with propranolol: improvement in anginal symptoms and exercise tolerance with combined drug therapy.

Twenty-nine patients symptomatic despite beta-blocker therapy were entered into a randomized, double-blind, placebo-controlled, crossover trial of lidoflazine added to propranolol. After clinically documented beta blockade was achieved, patients were randomized to either propranolol plus placebo (P) or propranolol plus lidoflazine (L). Patients initially receiving lidoflazine (group with treatment sequence LP) showed improvement in exercise tolerance from propranolol alone (7.2 to 9.3 minutes, p less than 0.05). Those randomized initially to propranolol plus placebo (group with treatment sequence PL) had unchanged exercise tolerance (7.3 minutes). After 4 months, patients were crossed over to the alternative form of therapy. Patients (group PL) now receiving lidoflazine in addition to propranolol increased their exercise duration (7.8 minutes), but not, significantly. However, patients switched to propranolol plus placebo (group LP) continued to sustain their improved exercise capacity, showing a "carryover" effect. Symptomatic improvement was manifested by a statistically significant reduction in both anginal attack rate and nitroglycerin consumption. The therapeutic efficacy of combined therapy was associated with further blunting of the heart rate response to exercise achieved by beta blockade alone. The combination of agents was well tolerated.

Angina Pectoris↗
PubMed1984

Prazosin versus propranolol plus prazosin: a comparison in diuretic-treated hypertensive patients.

The antihypertensive efficacy of prazosin was compared with that of a combination of prazosin and propranolol in 14 patients with essential hypertension. All patients had sitting diastolic blood pressures greater than or equal to 95 mm Hg despite daily therapy with 50 mg of hydrochlorothiazide and 240 mg of propranolol. After a 4-week monitoring period, patients were divided randomly into 2 groups in whom either (1) propranolol was reduced to 120 mg/day (to avoid potential hypotension) and prazosin was added, starting with an initial dose of 1 mg twice daily, or (2) propranolol was tapered and discontinued as prazosin was added. The average doses of prazosin were 7.4 and 7.6 mg/day, respectively. After 12 weeks of therapy, blood pressure was reduced in both groups, and there was no significant difference in the reduction of blood pressure or dose of prazosin in the 2 groups. Mean heart rate increased significantly in both groups (p less than 0.01), but more so in the group of patients who discontinued propranolol therapy. Thus, when a combination of 50 mg/day of hydrochlorothiazide and 240 mg/day of propranolol is insufficient to control hypertension, the addition of prazosin is shown to decrease blood pressure whether or not propranolol is continued.

Aged↗
PubMed1985

Cardiovascular and pharmacokinetic consequences of combined administration of verapamil and propranolol in dogs.

Verapamil and propranolol, alone and in combination, were given intravenously to anesthetized dogs to analyze the interaction between drug-induced cardiovascular effects and the resulting changes in pharmacokinetics. Dosing regimens were used that produced steady state plasma levels of both drugs, and the observed effects were clearly related to the plasma concentrations of the agents. When given alone, at stable "therapeutic" levels in plasma, verapamil or propranolol decreased spontaneous heart rate, increased atrioventricular conduction time, and had opposite effects on cardiac output. At the same doses, the combined infusion of the 2 drugs rapidly resulted in profound depression in cardiac function; in addition, plasma concentrations of both agents increased into ranges associated with cardiovascular toxicity. When verapamil doses were reduced, combined infusion with propranolol decreased atrioventricular conduction and cardiac output, but drug plasma concentrations (and associated effects) remained stable. When reduced doses of propranolol were added to infusion of verapamil, similar effects on cardiovascular function occurred, but plasma drug levels increased progressively throughout the remainder of the study period. In all combinations studied, beta blockade with propranolol decreased liver plasma flow and, therefore, the systemic clearance of verapamil. The in vitro effects of propranolol on verapamil metabolism were small, although significant, and not clinically relevant. These acute studies suggest that the hemodynamic effects resulting from verapamil and propranolol in combination may significantly diminish clearance of 1 or both drugs, thereby resulting in accumulation during continued administration, increased drug effects with increasing plasma concentrations, and potentially lethal drug toxicity.

Animals↗
PubMed1986

Calcium antagonists and beta blockers in the control of mild to moderate systemic hypertension, with particular reference to verapamil and propranolol.

The antianginal and antiarrhythmic role of calcium antagonists is well established. Recent preliminary studies have indicated that, like beta blockers, calcium antagonists may produce short- and long-term hypotensive effects in patients with mild to moderate essential hypertension. The pharmacologic properties of calcium antagonists provide a clear rationale for their use in the control of essential hypertension. The comparative hypotensive effects of verapamil (80 to 160 mg 3 times a day) and propranolol (40 to 120 mg 3 times a day) were evaluated over 4 weeks, preceded by a 4-week placebo phase, in a double-blind protocol in 17 patients with mild to moderate hypertension. Verapamil (n = 10) reduced the mean sitting systolic blood pressure by 10.7% (p less than 0.01) and standing by 7.6% (p less than 0.04). The corresponding data for propranolol (n = 7) were 4.8% (not significant) and 5% (p = 0.04). Verapamil reduced the sitting diastolic blood pressure by 10.8% (p less than 0.01), propranolol by 7.5% (p = 0.01); the standing diastolic blood pressure was reduced by 10.7% with verapamil (p less than 0.01) and by 8.6% (p = 0.01) with propranolol. With verapamil the mean heart rate fell from 77.60 +/- 8.42 to 70.20 +/- 4.85 beats/min (p = 0.03); with propranolol it fell from 76.85 +/- 6.91 to 66.29 +/- 4.54 beats/min (p less than 0.01). Although a trend towards a slightly greater hypotensive effect was apparent with verapamil compared with propranolol, the difference was not statistically significant. It is concluded that verapamil and propranolol exert comparable hypotensive potency in patients with mild to moderate hypertension.

Adrenergic beta-Antagonists↗
PubMed1989

Efficacy of intravenous propranolol for suppression of inducibility of ventricular tachyarrhythmias with different electrophysiologic characteristics in coronary artery disease.

The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed greater than or equal to 1 membrane-active antiarrhythmic drug (mean 2.2 +/- 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had greater than or equal to 1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29%) became noninducible (responders) and 17 patients (71%) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 +/- 14 vs 86 +/- 11 beats/min, p less than 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 +/- 14 to 80 +/- 9 beats/min, p less than 0.001) than in nonresponders (from 86 +/- 11 to 74 +/- 9 beats/min, p less than 0.01) (p less than 0.05 between the groups), despite equal plasma propranolol concentrations (84 +/- 50 vs 88 +/- 43 ng/ml, difference not significant). Seven of 11 patients (64%) who had greater than or equal to 1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after beta blockade (p less than 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 +/- 38 vs 302 +/- 66 ms, p less than 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.

Aged↗
PubMed1991

Comparison of celiprolol and propranolol in stable angina pectoris. Celiprolol International Angina Study Group.

The comparative antianginal effects and safety of propranolol and celiprolol, a highly beta 1-selective adrenoceptor blocker with selective partial beta 2-adrenoceptor agonist activity, were assessed in an international multicenter, placebo run-in, active control, double-blind, randomized, titration-to-effect study of 140 patients with stable, exercise-induced angina pectoris. At baseline, all patients received placebo for 2 weeks, then titrated doses of once-daily celiprolol (200, 400, 600 mg) or twice-daily propranolol (total daily dose 80, 160, 320 mg) over 4 weeks, followed by a 2-week maintenance period. Heart rate and blood pressure, at rest and with exercise, weekly anginal attack frequency, nitroglycerin consumption and symptom-limited treadmill exercise times (modified Bruce protocol) were assessed. Compared with their respective baselines, both celiprolol and propranolol reduced anginal attack and nitroglycerin consumption rates to a comparable degree, while improving exercise tolerance (p less than 0.05). Treatment with propranolol compared with celiprolol, however, was associated with a significantly lower heart rate at rest (p less than 0.01). The double-product at the conclusion of exercise testing was significantly reduced by both drugs. Celiprolol and propranolol had similar effects on blood pressure, and were well tolerated. More symptomatic bradycardia occurred with propranolol. Despite the differences in their hemodynamic actions, once-daily celiprolol is as effective as twice-daily propranolol in the treatment of patients with stable angina pectoris.

Adrenergic beta-Antagonists↗
PubMed1979

Propranolol therapy in thyrotoxicosis. A review of 84 patients undergoing surgery.

The effect of propranolol on the surgical course of 84 thyrotoxic patients undergoing partial thyroidectomy or extrathyroidal surgery was evaluated. Seventy-two patients (group 1) underwent surgery with propranolol as their sole preparatory medication, whereas in 12 (group 2) surgery was carried out after a rather prolonged period of thionamide preparation with the addition of propranolol preoperatively as an adjunctive therapeutic agent. Preoperative pulse rate and systolic blood pressure levels fell in both groups, and the clinical features of thyrotoxicosis were rapidly ameliorated with an average dose of propranolol of 330 mg (range 40 to 1,280 mg) daily. Maximal clinical response occurred within 48 to 72 hours of starting propranolol therapy. In 14 patients in group 1, paired serum calcium levels were reduced by the administration of propranolol preoperatively; serum thyroxine levels were unchanged. Serum thyroxine decay, evaluated postoperatively in the patients in group 1, was decreased. The half life of thyroxine was inversely related to the initial thyroxine levels. Analysis of these data indicates that the administration of propranolol alone provides rapid, safe and effective preparation of thyrotoxic patients for emergency or for elective thyroidal or extrathyroidal surgical procedures.

Adolescent↗
PubMed1981

Double-blind, randomized, placebo-controlled comparison of propranolol and verapamil in the treatment of patients with stable angina pectoris.

This study was performed to compare the relative efficacies of propranolol and verapamil in patients with stable angina pectoris. In 18 patients (16 men, two women, mean age 58 years) with coronary artery disease and angina of effort, the results of low (40 mg every 6 hours) and high-dose (80 mg every 6 hours) propranolol therapy were compared to those of low (80 mg every 6 hours) and high-dose (120 mg every 6 hours) verapamil therapy in a double-blind, randomized, placebo-controlled evaluation which lasted eight weeks: two weeks of placebo therapy, two weeks of propranolol or verapamil (one week low-dose, one week high-dose) therapy, three days of down-titration followed by one week of placebo therapy, two weeks of propranolol or verapamil therapy (whichever was not given earlier in the trial) (one week low-dose, one week hgh-dose) and three days of down-titration. During each period the following were quantitated: (1) chest pains/week; (2) nitroglycerin used/week; (3) transient ischemic S-T segment deviations and highest grade of ventricular ectopic activity on two-channel Holter monitor; (4) S-T segment deviations during supine bicycle exercise; (5) left ventricular volumes and ejection fraction at rest and during exercise (assessed by equilibrium gated blood pool scintigraphy); and (6) pulmonary function studies. Propranolol and high-dose verapamil therapy significantly reduced the frequency of angina, and high-dose verapamil therapy diminished both the need for nitroglycerin and the frequency of transient ischemic S-T segment deviations on Holter monitor. Neither agent exerted a clinically-important deleterious influence on left ventricular volumes or the ejection fraction. Forced vital capacity and forced expiratory volume were worsened by propranolol but not by verapamil. Thus, in the patient with angina of effort, verapamil is a satisfactory therapeutic alternative to propranolol.

Adult↗
PubMed1993

The effect of propranolol on salivary gland function and dental caries development in young and aged rats.

Medications commonly used in elderly people cause hyposalivation and are associated with an enhanced prevalence of dental caries. Propranolol (a beta-adrenergic antagonist) is a commonly used antihypertensive agent that is prescribed for long-term use. The purpose of this investigation was to compare the effects of this drug on salivary composition and flow rate, and on caries, in young and aged rats. Forty young (28-day) and 36 aged (20-month) female Sprague-Dawley rats were infected with Streptococcus sobrinus 6715 and fed a cariogenic diet for 28 days. Propranolol was given in high (20 mg/kg/day) and low (10 mg/kg/day) doses via osmotic pumps. Unoperated and desalivated animals served as controls. Smooth-surface caries scores in the young animals receiving propranolol at 20 mg/kg/day were statistically higher than in the young intact rats (p < or = 0.05). Increased smooth-surface and sulcal caries scores were recorded in the aged propranolol-treated animals, but the differences were not statistically significant when compared with those in intact aged animals. Propranolol in aged animals did not affect the amount of alveolar bone loss but increased the risk of development of root caries. Young animals harboured greater populations of Strep. sobrinus and total cultivable flora than did all aged groups except the desalivated group. Salivary flow rates, induced by pilocarpine, were not decreased by the chronic administration of propranolol. Although the total protein concentration in parotid and submandibular saliva from drug-treated animals was reduced, differences were not observed in their SDS-PAGE profile when compared with unoperated animals. The findings demonstrate that chronic use of propranolol reduced the total protein concentration in saliva of all animals, increased caries susceptibility, but did not reduce the stimulated salivary flow rate.

Aging↗