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PubMed1999

Propranolol in hypoglycaemia unawareness.

The effect of propranolol on the occurrence of hypoglycaemic symptoms was assessed in insulin-dependent diabetic patients with hypoglycaemia unawareness. A double-blind, randomised parallel group study (2:1 fashion) was conducted over 4-week period. The propranolol group (n = 9) received 20 mg (week 1 and 2) and 30 mg (week 3 and 4) twice daily, and the other group (n = 5) a matched placebo for 4 weeks. Patients included had experienced at least two severe hypoglycaemic episodes (coma or seizures) during the previous year, which were characterised by a lack of adrenergic symptoms and required the assistance of another person. The mean number of hypoglycaemias during the study period was similar in both groups (placebo: 13 +/- 2 propranolol: 11 +/- 1), whereas the number of totally asymptomatic hypoglycaemias (< 0.6 g/l) was lower on propranolol than on placebo (3 +/- 1 vs 8 +/- 3, NS) and the number of symptomatic hypoglycaemias was higher (7.2 +/- 2 vs 4.6 +/- 1, NS). Subjective evaluation of treatment by the investigators showed 0/5 successes in the placebo group and 5/9 in the propranolol group (chi2 = 4.32, p = 0.038). The main advantage of propranolol over placebo was an increased incidence of sweating. The ratio [number of hypoglycaemias with sweating/total number of hypoglycaemias] being higher with propranolol (0.28 +/- 0.08 vs 0.06 +/- 0.02, p = 0.06). This pilot study suggests that beta-blockers may be useful in restoring adrenergic symptoms during hypoglycaemia in insulin-dependent diabetic patients without warning symptoms of hypoglycaemia. This beneficial effect seems to be predominantly related to an increase in hypoglycaemia-induced sweating. A larger study is needed to confirm or invalidate these preliminary results.

Adrenergic beta-Antagonists↗
PubMed1998

The effect of propranolol versus placebo on resident surgical performance.

PURPOSE: To determine whether propranolol can decrease surgical tremor and anxiety in residents performing ocular microsurgery without impairing patient or physician safety. METHODS: In this randomized, double-masked, crossover study, 5 third-year ophthalmology residents ingested a capsule containing either propranolol, 40 mg, or placebo 1 hour prior to performing ophthalmic microsurgery. All residents were healthy men under age 30 years. Prior to commencement of the study, all participants had successfully been administered a test dose of propranolol without side effects. The study took place over a 10-week period. At the conclusion of each case, both the resident and attending surgeon observer independently completed a form grading, on a sliding scale: (1) amount of overall tremor; (2) amount of tremor during placement of the first 3 sutures after lens or nucleus extraction; (3) anticipated difficulty of the case; (4) actual difficulty with the case; and (5) anxiety (surgeon only). In addition, the type of procedure performed, complications encountered, and surgeon side effects were recorded. The data were analyzed with a 2-way analysis of variance for unbalanced data. RESULTS: A total of 73 surgical cases were performed; the surgeons were administered propranolol for 40 cases and placebo for 33. As judged by the resident surgeon, there was a highly significant effect of propranolol in decreasing anxiety (P = .0058), reducing surgical tremor overall (P < .0001), and reducing tremor while placing the first 3 sutures following lens extraction (P < .0001). There was no treatment-by-surgeon interaction for any of the measures. Complications and difficulty of the case, as judged by both the resident and attending surgeons, were not significantly different in the propranolol versus placebo groups (P > .05). There were no side effects reported or observed in any of the surgeons. CONCLUSIONS: Propranolol, 40 mg, administered 1 hour prior to surgery, significantly decreases tremor and anxiety in the surgeon without untoward effects to the surgeon and the patient. However, it is unknown whether decreased tremor and anxiety improved surgical outcome.

Adrenergic beta-Antagonists↗
PubMed2000

Effect of thromboxane synthase inhibitor, CS-518, on propranolol-induced bronchoconstriction in guinea pigs.

Beta-adrenoreceptor antagonists, such as propranolol, can provoke severe bronchoconstriction in asthmatic subjects. Recently we developed an animal model of propranolol-induced bronchoconstriction and investigated the involvement of chemical mediators in this reaction. The purpose of this study was to elucidate the role of thromboxane A2 in the development of propranolol-induced bronchoconstriction after allergic bronchoconstriction. Passively sensitized guinea pigs were anesthetized and treated with diphenhydramine hydrochloride and were then artificially ventilated. Propranolol at a concentration of 10 mg/ml was inhaled 20 min after an aerosolized antigen challenge. A potent and selective thromboxane A2 synthase inhibitor, CS-518, in doses of 0.01, 0.1 and 1 mg/kg and vehicle were administered intravenously 15 min after the antigen challenge. Another study was performed in naive guinea pigs; ascending doses of methacholine (12.5, 25, 50, 100 and 200 microg/ml) were inhaled for 20 sec at 5-min intervals, 10 min after intravenous administration of CS-518. Propranolol inhaled 20 min after the antigen challenge caused bronchoconstriction in sensitized guinea pigs. CS-518 administered 15 min after the antigen challenge significantly inhibited propranolol-induced bronchoconstriction in a dose-dependent manner, while CS-518 did not influence the dose-dependent response to inhaled methacholine in naive guinea pigs. We conclude that thromboxane A2 contributes to the development of propranolol-induced bronchoconstriction following allergic reaction in our guinea pig model.

Adrenergic beta-Antagonists↗
PubMed1975

Protective role of increased myocardial glycogen stores induced by propranolol.

Glycogen is an essential substrate during myocardial anoxia. Since porpranolol may maintain myocardial glycogen levels after acute stress by blockade of catecholamine-induced glycogenolysis, we evaluated the effect of propranolol treatment in the isolated perfused isovolumic paced rat heart. Forty-one rats were studied after 10 min of ice-water immersion: half were pretreated with propranolol, 20 mg/kg/day x3, and half with saline. Glycogen content of unperfused propranolol-treated hearts exceeded controls by 46% (146 +/- 9 vs. 100 +/- 4 mumoles/g dry wt, p less than 0.02), and this difference persisted during aerobic perfusion. Propranolol did not affect adenine nucleotide concentration or left ventricular hemodynamics. Following 5 min of anoxic perfusion, propranolol hearts showed improved ventricular performance concomitant with enhanced glycogenolytic flux and lactate production. Propranolol augmented high energy phosphate production (ATP/AMP = 5.19 +/- 0.42 vs. 3.39 +/- 0.42, p less than 0.02) and increased coronary flow (22.1 +/- 1.6 vs. 16.6 +/- 1.4 ml/min, p less than 0.02) during anoxia. Thus, propranolol supported glycogen stores following acute stresses, enhanced glycogenolytic energy production, increased coronary flow, and improved ventricular function during subsequent anoxia.

Animals↗
PubMedDate not supplied

Hemodynamic effect of spironolactone in liver cirrhosis and propranolol-resistant portal hypertension.

OBJECTIVE: In a proportion of patients with liver cirrhosis, portal pressure does not decrease adequately with propranolol. These patients may benefit from another drug that may reduce portal pressure. We evaluated the role of spironolactone, alone or with propranolol, in such patients. METHODS: Patients with cirrhosis, with or without ascites, with esophageal varices and with hepatic venous pressure gradient exceeding 12 mmHg, which did not show a 20% reduction after an 80-mg oral dose of propranolol, were studied. They were allocated to receive spironolactone 100 mg orally once daily either alone (group 1, n=10) or with propranolol 40 mg orally twice daily (group 2, n=10), for 7 days, after which the hemodynamic study was repeated. RESULTS: Hepatic venous pressure gradient decreased in those receiving spironolactone and propranolol (p=0.007); 5 patients in group 1 and 7 in group 2 showed a reduction in hepatic venous pressure gradient by more than 20%. However, the reduction produced by spironolactone alone (20.5 [31.3]%) was not significantly different from that produced by combination therapy (30.3 [25.9]%; p=0.46). CONCLUSION: Spironolactone in combination with propranolol achieves adequate reduction (> or = 20%) in hepatic venous pressure gradient in propranolol-resistant portal hypertension in patients with liver cirrhosis. Spironolactone alone was also effective in some patients.

Adrenergic beta-Antagonists↗
PubMed1976

Beta-adrenergic receptors and the effect of beta-adrenergic blocking agent propranolol on histamine and reserpine stimulated gastric acid secretion in man: normals and duodenal ulcer cases.

The effects of the beta adrenergic stimulant drug, "Nylidrin", and the beta adrenergic blocking agent, "Propranolol", on human basal gastric acid secretion were studied in 20 healthy volunteer subjects and 10 chronic D.U. cases. Nylidrin increased gastric acid secretion and volume. All effects of nylidrin were blocked by prior administration of beta adrenergic inhibitor propranolol. Propranolol diminished both acid secretion and volume in both normal and D.U. cases. The presence of beta adrenergic receptors in the human stomach was suggested. The effects of beta adrenergic blocking agent propranolol on gastric secretion, stimulated with histamine, were studied in 10 normal subjects and 10 cases of chronic duodenal ulcer patients. Pretreatment with propranolol produced a signigicant depression of the 90 minute acid response to histamine in both volume and acidity in normals and duodenal ulcer cases. It is concluded that propranolol has an antisecretory effect, not only on basal gastric secretion but also on histamine stimulated secretion in man. Reserpine stimulated gastric acid secretion and volume in normals but showed no similar effect in D.U. cases. After pretreatment with propranolol it reduces the gastric acid secretion and volume in normals and D.U. cases.

Adult↗
PubMedDate not supplied

Stereoselective differences in propranolol disposition in female Sprague-Dawley and Dark Agouti rats.

Although genetic constitution is recognized as an important factor in drug elimination, there is still only a modest amount of information about its impact on stereoselective drug disposition. To examine how strain differences in cytochrome P-450 expression may affect stereoselective drug elimination, the disposition of R- and S-propranolol was examined in female Sprague-Dawley (SD) and Dark Agouti (DA) rats. The half-life of R-propranolol was increased and its apparent oral clearance decreased significantly in DA rats relative to the SD strain [85 +/- 41 min (DA) vs. 26 +/- 10 min (SD) and 0.020 +/- 0.014 liter/min/kg (DA) vs. 0.31 +/- 0.14 liter/min/kg (SD)], respectively. Strain differences in S-propranolol half-life and apparent oral clearance also were observed, but were not as marked [97 +/- 36 min (DA) vs. 52 +/- 35 min (SD) and 0.20 +/- 0.13 liter/min/kg (DA) vs. 0.70 +/- 0.68 liter/min/kg (SD)], respectively. Due to a more pronounced effect of rat strain on the disposition of R-propranolol, the stereoselective S-/R- oral clearance ratio for propranolol was also strain-dependent [10 +/- 3 (DA) vs. 2.1 +/- 0.9 (SD)]. These differences could not be accounted for by propranolol stereoselective plasma protein binding or by a difference in the blood/plasma ratio for R- or S-propranolol in these separate strains. This represents one of the few examples where an increase in stereoselective drug disposition has been observed due to strain differences that diminish drug elimination.

Animals↗
PubMed1991

Lack of efficacy of d-propranolol in neuroleptic-induced akathisia.

d-Propranolol lacks clinically significant beta-adrenergic receptor blocking properties, but has the same membrane stabilizing effects as racemic (d,l) propranolol. To assess the role of beta-blockade versus membrane stabilization or other shared nonspecific effects in the therapeutic action of propranolol in neuroleptic-induced akathisia (NIA) we treated 11 patients with NIA in a crossover, double-blind study of d-propranolol versus placebo. Akathisia scores were unchanged after both d-propranolol and placebo. Eight patients were subsequently treated in a nonblind manner with racemic propranolol, with a significant reduction in akathisia scores. These findings suggest that beta-blockade, not membrane stabilization or other shared nonspecific effects, contributes to the efficacy of propranolol in NIA.

Adult↗
PubMed2006

Increased serotonergic functions following adminstration of 1-(1-naphthyl) piperazine in propranolol injected rats.

Propranolol a beta adrenergic antagonist, binds with 5-HT1 receptor. 1-(1-naphthyl) piperazine (1-NP) a derivative of quipazine has serotonin antagonist activity at 5-HT2 and agonist activity at 5-HT1 site. In the present study neurochemical and behavioral effects of 1-NP was monitored in saline and propranolol injected rats. 1NP increased locomotor activity in saline as well as in propranolol injected rats. Administration of propranolol also increased locomotor activity and these increases were more enhanced following 1-NP administration. Levels of 5-HT were not altered following the administration of 1NP in saline as well as propranolol injected rats. 5-HT turnover however decreased by the administration of propranolol Adminstration of 1NP decreased 5-HT turnover in saline but not in propranolol injected rats.

Adrenergic beta-Antagonists↗
PubMed1976

Inhibition by propranolol of bile acid stimulation of rabbit colonic adenylate cyclase in vitro.

UNLABELLED: Bile acids, especially unconjugated deoxycholic acid, cause diarrhea by inducing colonic mucosal secretion of water and electrolytes. This effect has been shown to be mediated by adenylate cyclase (AC). Propranolol, a beta-adrenergic blocking agent which inhibits AC, may then prevent this action of bile acids on colonic mucosa. The aim of this study was to determine the effect of bile acids, catecholamines, and propranolol on AC activity in colonic mucosa. The in vitro effects of deoxycholic acid, taurocholic acid, NaF, epinephrine, norepinephrine, and propranolol on AC in rabbit colonic mucosa were determined. NaF, 10(-4) M, increased AC activity to 220% of control (P less than 0.01). Deoxycholic acid, 10(-4) M, increased AC activity to 178% of control (P less than 0.01). Lesser but significant (P less than 0.01) stimulation of AC occurred at both higher and lower concentrations of deoxycholic acid, with no effect at 10(-10) M. Taurocholic acid, 10(-4) M, and epinephrine and norepinephrine, 10(-2) M, 10(-4) M, 10(-6) M, and 10(-8) M, had no effect on AC. Propranolol, 10(-6) M, caused a 60% decrease (P less than 0.01) in the stimulated AC activity induced by 10(-4) M deoxycholic acid. Propranolol, 10(-4) M, decreased basal AC by 30% (P less than 0.01). IN CONCLUSION: (1) Deoxycholic acid, but not taurocholic acid, epinephrine, or norepinephrine, stimulates colonic AC activity. (2) Propranolol inhibited this deoxycholic acid stimulation of AC. (3) Catecholamines are not intermediaries in this action of propranolol on colonic mucosal AC activity.

Adenylyl Cyclase Inhibitors↗
PubMed1991

[Comparison of the characteristics of methacholine and of propranolol in the assessment of aspecific hyperreactivity of the airways].

Quantitative bronchial challenge tests with methacholine and propranolol were performed in volunteers with bronchial asthma (n = 17) and in normal controls (n = 13), in order to test the earlier assumption that propranolol might be more useful to assess nonspecific bronchial responsiveness in bronchial asthma. The investigations were performed in random order, with a minimum interval of 24-hours. The aerosol was administered by a dosimeter (APS, Jaeger), using doubling concentrations, with a maximum of 25 mg/ml (2.5%), the lowest concentrations being 0.26 mg/ml (propranolol) and 0.03 mg/ml (methacholine), respectively. The provocation dose at a decrease in sGaw of 50% (PD50) was calculated from the dose-response curve. While methacholine induced an airways obstruction sufficient to calculate a PD50 in 29/30 subjects, propranolol was similarly effective in only 19/30 cases the rank correlation coefficient was 0.4368 (p less than 0.025). At a methacholine-PD50 greater than 0.2 mg(= concentration greater than 1 mg/ml) no propranolol-PD50 could be determined. In accordance with the literature, in the asthmatic subgroup the PD50sGaw [geometric means] were 25 (2.7-109.6) micrograms for methacholine, and 900 (75.9-3331) micrograms for propranolol, or 0.13 mumol and 3.46 mumol, respectively. The inhalation of propranolol in the highest possible concentration (limited solubility) induced airways obstruction only in subjects with asthmatic hyper-responsiveness. A similar distinction between asthmatic and normal subjects is possible by methacholine using a threshold concentration (in this study: cumulative PD50sGaw 0.2 mg or provocation concentration 1 mg/ml). Moreover, methacholine allows a determination of minor degrees of hyperresponsiveness, in mild airways obstruction or normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[Specific and nonspecific effects of beta receptor blockers: stereoselectively different properties exemplified by (R)- and (S)-propranolol].

Beta adrenoceptor antagonists bind specifically to beta receptors in a reversible way, so they inhibit beta stimulating actions of beta mimetics such as epinephrine, norepinephrine, isoprenaline, etc. The effect of beta adrenoceptor antagonism depends on the extent of sympathetic activity and is most pronounced during work and stress. Most beta blockers are administered as racemic mixtures consisting of 50% of the (R)- and 50% of the (S)-enantiomer, but only one enantiomer (e.g. (S)-propranolol) exerts beta blocking activity in therapeutic doses while the other one (e.g. (R)-propranolol) does not. But there is also a number of non-beta blocking actions of beta adrenoceptor antagonists that show variable stereoselectivity. Propranolol is explored most extensively in this field: 1. Only (R)-propranolol inhibits the conversion of thyroxine to triiodothyronine. 2. Both (R)- and (S)-propranolol exert class 1 antiarrhythmic activity. 3. Both (R)- and (S)-propranolol decrease the intraocular pressure. In all these indications mentioned above, beta blockade as an unwanted effect could be avoided by administering optically pure (R)-propranolol instead of the racemic mixture. Stereoselectivity does not only influence the effects but also metabolism, protein-binding etc. of beta adrenoceptor antagonists. In fact, the (R)- and the (S)-enantiomer of a beta adrenoceptor antagonist are 2 substances with different pharmacodynamic and pharmacokinetic properties. Nevertheless, they are currently used as racemic mixtures in research as well as in therapy without being aware of stereoselective implications although there are nowadays methods available to separate and isolate the optically pure enantiomers of most beta adrenoceptor antagonists with high purity and on large scale at reasonable costs.

Adrenergic beta-Antagonists↗
PubMed1990

Effects of diltiazem or propranolol during exercise training of hypertensive men.

This was a prospective, randomized, double-blind, placebo-controlled trial to establish whether beta blockers or calcium-channel blockers limit exercise capacity and training responses in men with mild hypertension. Circuit weight and aerobic training was used to assess the effects of drugs on cardiovascular fitness and muscle strength. Fifty-two sedentary men, ages 25-59 yr, with a diastolic blood pressure of 90-105 mm Hg off drugs, without significant ST depression during maximal stress testing, received diltiazem, propranolol, or placebo. Maximal oxygen uptake (VO2max) and exercise duration during treadmill testing, as well as one-repetition maximal strength, were assessed on eight weight machines after a single-blind placebo baseline, after 2 wk of drug run-in, and after 10 wk of exercise training. Total daily doses were 240 mg for propranolol and 360 mg for diltiazem. Propranolol decreased VO2max after drug run-in (P less than 0.05). Exercise training increased VO2max (P less than 0.05) in the diltiazem and placebo groups. After training VO2max in the propranolol group increased (P less than 0.05) from run-in but not beyond baseline levels. Thus, the reduction of VO2max consequent to propranolol therapy limited the overall benefits of training. Exercise duration did not change with run-in and increased (P less than 0.05) with training by 22%, 19%, and 10% for the diltiazem, placebo, and propranolol groups, respectively. Strength after run-in was unchanged, and exercise training increased strength (P less than 0.0001) on all weight machines in all groups. The results show an advantage of diltiazem to propranolol, particularly among physically active patients engaged in aerobic exercise who require antihypertensive therapy.

Adolescent↗
PubMed1989

Negative chronotropic actions of sufentanil and vecuronium in chronically instrumented dogs pretreated with propranolol and/or diltiazem.

Patients with ischemic heart disease who present for surgery are frequently managed with a "high dose" narcotic technique utilizing fentanyl or sufentanil in combination with neuromuscular blockade. Narcotic anesthetic induction has been associated with perioperative cardiac conduction disturbances, particularly in patients previously treated with calcium channel and/or beta-adrenergic antagonists. The purpose of the present investigation was to examine in chronically instrumented dogs the effects on systemic and coronary hemodynamics and regional contractile function of sufentanil alone or in combination with the nondepolarizing neuromuscular blocking agent vecuronium, with and without pretreatment with the calcium channel blocking agent diltiazem, and/or the beta-adrenergic antagonist propranolol. Thirty-six experiments were conducted in four groups of 19 chronically instrumented dogs. Administration of sufentanil (25 and 50 micrograms/kg of normal body weight IV) resulted in a significant sinus or junctional bradyarrhythmia without alteration in systemic and coronary hemodynamics. Pretreatment with propranolol (1 mg/kg IV) decreased left ventricular +dP/dt without other hemodynamic alterations. After propranolol pretreatment, sufentanil (25 and 50 micrograms/kg IV) produced statistically significant dose-dependent decreases in heart rate and +dP/dt, while increasing mean and diastolic coronary vascular resistances. After pretreatment with diltiazem (0.3 mg/kg IV) and propranolol (1.0 mg/kg IV), sufentanil (25 micrograms/kg IV) produced significantly greater bradycardia (38 +/- 4 beats/min) than it did in non-pretreated or propranolol-pretreatment dogs. Similarly, administration of sufentanil (25 micrograms/kg IV) in combination with vecuronium (0.1 mg/kg IV) after propranolol and diltiazem pretreatment resulted in the appearance of bradyarrhythmias (32 +/- 2 beats/min) and two episodes of asystole, responsive to atropine sulfate (0.4 mg). In spite of severe bradycardia, arterial pressure was well maintained in all groups. In all groups, administration of naloxone (0.2 mg/kg IV and 0.2 mg/kg IM) after sufentanil produced significant increases in arterial pressure, left ventricular +dP/dt, and diastolic coronary blood flow velocity. Therefore, the combination of sufentanil and vecuronium in chronically instrumented dogs may result in the appearance of cardiac conduction disturbances. This action is more likely to occur after pretreatment with diltiazem and propranolol. Although systemic hemodynamics were well maintained in dogs in the present study during the episodes of bradyarrhythmias, potentially significant cardiovascular deficits may occur in pa

Analgesics↗
PubMedDate not supplied

Pharmacokinetics and metabolism of a 4'-methylthio derivative of propranolol in the dog.

The purpose of this study was to examine the effect of a methylthio substituent in the metabolically most active position of propranolol, i.e. the 4'-position, on the pharmacokinetics and metabolism of this drug in the dog. The kinetics of 4'-methylthiopropranolol (MTP) were compared to those of propranolol following simultaneous iv doses of labeled drug and oral doses of unlabeled drug. MTP had a significantly larger volume of distribution and a longer half-life, and demonstrated a greater accumulation by red blood cells and cardiac conductile tissue than propranolol, effects which presumably are due to a higher lipophilicity of MTP. The greatest effect was on the oral clearance, which was substantially lower for MTP (1.6 vs. 5.5 liters/min) with an associated higher bioavailability (23.1 vs. 10.9%). Studies of MTP metabolism using radiolabeled drug showed that MTP, like propranolol, was eliminated entirely by metabolism. About 70% of the urinary radioactivity was extractable into ethyl acetate at pH 9.8 and pH 2.0. The extractable metabolites were separated by HPLC and identified by GC/MS, direct probe MS, and comparison with authentic compounds. Eleven metabolites were identified as sulfoxides and, in particular, sulfones of MTP and its N-dealkylated and subsequently deaminated glycollic and lactic acid metabolites. The nonextractable urinary radioactivity (30%) was isolated by DEAE-Sephadex chromatography and identified by HPLC/MS as four glucuronic acid conjugates. In contrast to propranolol, there was no evidence of aromatic carbon oxidation for MTP. These observations suggest that the markedly decreased oral clearance of MTP compared to propranolol is due to qualitatively altered metabolism from a highly efficient aromatic carbon oxidation for propranolol to a less efficient sulfur oxidation for MTP.

Animals↗
PubMed1989

Pulmonary extraction of propranolol in normal and oxygen-toxic sheep.

To help define the mechanisms involved in the handling of propranolol by normal and injured lungs, we studied the pulmonary extraction of [3H]propranolol in 23 unanesthetized sheep. Extraction of propranolol by normal lungs during a single circulation was characterized by 1) subsequent back-diffusion and pulmonary retention of the drug, 2) no evidence of saturable uptake or binding, 3) no effect of isoproterenol or imipramine, and 4) no effect of increasing cardiac output by treadmill exercise. In lungs damaged by oxygen toxicity, [3H]propranolol extraction decreased progressively to 63% of base line, paralleling progressive arterial hypoxemia and hypercapnia. In contrast, [14C]serotonin extraction remained unchanged from base line. Our results suggest that in normal unanesthetized sheep, pulmonary extraction of propranolol occurs primarily by passive diffusion that is flow-limited. Also, lung injury induced by oxygen toxicity in sheep reduces the pulmonary extraction of propranolol. Indeed, in oxygen toxicity, the depressed extraction of propranolol is a more sensitive marker of lung injury than is serotonin extraction.

Animals↗
PubMed1989

The preoperative use of iodine solution in thyrotoxic patients prepared with propranolol. Is it necessary?

Despite the numerous reports documenting the safety and efficacy of the use of propranolol, a selective beta-adrenergic blocker, as the sole agent for preoperative preparation of a hyperthyroid patient, many surgeons continue to add a solution containing iodine to the treatment regimen. The rationale for the concomitant use of iodine solution and propranolol is that the iodine solution reduces the amount of propranolol required to make the patient symptomatically euthyroid and that iodine administration reduces the vascularity of the gland, thereby minimizing intraoperative blood loss. To ascertain the validity of these beliefs, we retrospectively reviewed our experience with 42 consecutive hyperthyroid patients who underwent subtotal thyroidectomy. These patients either received propranolol alone (20 patients) or propranolol with iodine solution (22 patients) for preoperative preparation. Comparison of the medication doses, estimated blood loss, and postoperative changes in hemoglobin and hemocrit using the Student's t-test, failed to demonstrate any significant difference between the two treatment protocols (P greater than 0.1). We conclude that the addition of iodine to propranolol for preoperative preparation of hyperthyroid patients does not result in any significant advantage over the use of propranolol alone.

Administration, Oral↗
PubMed1985

Lack of effect of propranolol on the steady-state plasma levels of ketanserin.

The effect of propranolol treatment on the steady-state plasma levels of ketanserin was evaluated in 6 patients suffering from borderline hypertension and in 2 healthy volunteers. All subjects received ketanserin 40 mg b.i.d. for 21 days. From day 8 to 14 of the study propranolol was given additionally in a dose of 80 mg bid. This dose of propranolol had to be reduced in 3 subjects because of side effects. Steady-state plasma concentrations (measured 4-6 h after the dose) of ketanserin varied from 51.0 +/- 13.6 to 67.8 +/- 13.8 ng/ml (mean +/- SEM) during the entire study period. Treatment with propranolol (plasma concentrations ranged from 45.7 +/- 15.8 to 65.7 +/- 11.4 ng/ml) did not significantly alter the plasma concentrations of ketanserin. The same was true for the minimal plasma concentrations of ketanserin measured at the end of each treatment period. Blood pressure decreased during the 21 days treatment period with ketanserin (mean systolic blood pressure decreased from 144 +/- 5 to 123 +/- 7 and diastolic from 81 +/- 3 to 72 +/- 5 mmHg). Propranolol had a slight additional hypotensive effect. Heart rate decreased during treatment with propranolol. It is concluded that simultaneous oral treatment with propranolol in doses up to 160 mg/day does not alter the first-pass metabolism and the elimination kinetics of ketanserin.

Adult↗