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PubMed1993

Effect of oral activated charcoal on propranolol pharmacokinetics following intravenous administration to rabbits.

The pharmacokinetics of propranolol following intravenous administration (1 mg/kg), with and without treatment with oral activated charcoal, was investigated in rabbits. In charcoal-treated rabbits a significant reduction in propranolol serum concentrations was observed compared to control animals. Charcoal treatment significantly reduced the half-life of elimination (16.6%) and the mean residence time (19%) of propranolol. A 17% increase in the systemic clearance and a 14% decrease in AUC were also noted. Charcoal administration did not significantly alter the volume of distribution (Vc' V(area) and Vss) or the apparent distribution half-life. A two-compartment model adequately described propranolol in control and treated rabbits. The results indicate that administration of oral activated charcoal enhances the systemic elimination of propranolol. This is presumably mediated by interruption of the enterohepatic circulation of propranolol by activated charcoal.

Administration, Oral↗
PubMedDate not supplied

Temporal relationship between cardiac performance and myocardial uptake of dl-propranolol in man.

1. The temporal relationship between the myocardial arteriovenous difference of plasma propranolol concentration and heart rate and left ventricular dp/dt maximum was examined for 30 min after intravenous administration of 10mg (0.04 mmol) dl-propranolol in nine patients with ischaemic heart disease. 2. Very large positive myocardial a.v. differences of propranolol within the first 5 min became negative after 5 min, indicating a rapid, avid uptake with subsequent release of propranolol from the heart. 3. The heart rate and left ventricular dp/dt maximum increased 1 min after propranolol administration and did not change after the fifth min of the observation period. 4. The data suggest that a large number of unspecific binding sites for propranolol are present in the heart in addition to the specific beta-receptors.

Adult↗
PubMedDate not supplied

Nipradilol, a new beta-blocker with vasodilatory properties, in experimental portal hypertension: a comparative haemodynamic study with propranolol.

The haemodynamic effects of nipradilol, a new non-selective beta-adrenoreceptor blocker with vasodilating actions like nitroglycerin, were examined in rats with portal hypertension due to portal vein stenosis. Portal hypertensive rats were divided into five groups receiving infusion of placebo, 3 mg of propranolol, 300, 600 and 1200 micrograms of nipradilol. At its highest dose, nipradilol achieved a reduction of 34.4 +/- 4.4% in heart rate which was similar to that in the propranolol group (36.5 +/- 2.4%). Also for other systemic haemodynamic parameters, the nipradilol 1200 micrograms group exhibited changes not significantly different from those in the propranolol group; mean arterial pressure (-13 vs -14%), cardiac index (-37 vs -31%) and systemic vascular resistance (+29 vs +32%). In contrast to the similar changes in the systemic circulation, a 1200 micrograms dose of nipradilol lowered portal pressure significantly more than propranolol (-4.3 +/- 0.6 vs -2.9 +/- 0.2 mmHg, P < 0.05). Nipradilol then reduced portal blood flow by 22% (P < 0.05) without a significant change in portocollateral resistance. On the other hand, propranolol not only caused a reduction in portal blood flow of 30% (P < 0.01), but also an increase in portocollateral resistance of 21% (P < 0.05). The results suggest that nipradilol may ensure a more effective control of portal hypertension than propranolol, presumably via its venodilatory action on portocollateral vessels.

Adrenergic beta-Antagonists↗
PubMed1983

Reversibility of propranolol-induced changes in the biosynthesis of monoacylglycerol, diacylglycerol, triacylglycerol, and phospholipids in the retina.

The biosynthesis and metabolism of phospholipids and neutral glycerides were studied in the bovine retina. Radioactive glycerol was used as a precursor. Phentolamine and d- and dl-propranolol were found to produce similar effects on lipid metabolism in the retina. Marked stimulation of phosphatidylinositol (PhI) synthesis and maximal inhibition of phosphatidylcholine (PhC), diacylglycerol (DG), and triacylglycerol (TG) formation were observed within 5 min after exposure to 0.5 mM dl-propranolol. Pulse-chase experiments showed a high turnover rate in DG and a reversibility of the propranolol-induced changes produced during the synthesis of PhC, TG, DG, monoacylglycerol (MG), and phosphatidylserine. All reversals of the drug-induced biosynthetic profiles approached control values 60 min after incubation in drug-free medium. However, complete reversal was not achieved in any of the cases under these conditions. Propranolol appeared to inhibit both the formation of DG from phosphatidic acid and the further metabolism of DG, probably to MG. Phosphatidylethanolamine biosynthesis showed some recovery from this inhibition. Synthesis of PhI was greatly stimulated by preincubation with propranolol and was further enhanced by reincubation in the presence of propranolol. However, this effect was not reversed by reincubation without the drug. The active de novo biosynthesis of retinal phospholipids and glycerides is a very dynamic pathway that may be redirected by amphiphilic drugs. In addition, the partial reversal of modifications induced in the flux of [2-3H]glycerol through the lipids can occur during short-term reincubations of retinas in drug-free medium.

Animals↗
PubMed1995

beta-Adrenoceptor regulation in rat heart, lung and skin after chronic treatment with (--)-tertatolol or (--)-propranolol.

1. The effect of long-term treatment with the beta-adrenoceptor antagonists (--)-tertatolol and (--)-propranolol was studied. Sprague-Dawley rats were treated with either (--)-tertatolol (50 micrograms kg-1 hr-1), (--)-propranolol (250 micrograms kg-1 hr-1) or vehicle (1 mM HCl) for 14 days with osmotic minipumps implanted subcutaneously. 2. The mean daily systolic blood pressure and heart rate of rats treated with either (--)-tertatolol (108 +/- 1 mmHg/330 +/- 3 bpm) or (--)-propranolol (103 +/- 1 mmHg/330 +/- 2 bpm) were lower than in the control (126 +/- 1 mmHg/405 +/- 3 bpm, P < 0.001, n = 8-10) indicating the effectiveness of drug delivery. 3. Autoradiographic studies in areas of heart, lung and skin showed that beta-adrenoceptor populations were not significantly affected by the drug treatment (all regions P > 0.05). Nevertheless, the receptor population in the homogenates of (--)-tertatolol treated lung were halved (194 +/- 28 fmol mg protein-1 compared with a control value of 388 +/- 54 fmol mg protein-1, P < 0.01, n = 6). 4. In the presence of CGP 20712A, the left atrial inotropic and right atrial chronotropic responsiveness to (--)-isoprenaline were hypersensitive in both (--)-tertatolol and (--)-propranolol-treated groups (P < 0.005, ANCOVA). 5. (--)-Propranolol treated left ventricular free wall had lower basal [3H]-forskolin binding to adenylate cyclase (14.45 +/- 1.20 fmol mg protein-1 compared with a control value of 18.91 +/- 0.78 fmol mg protein-1, P = 0.01, n = 6). (--)-Tertatolol treatment had no effect on the basal binding. In the presence of the G-protein activators NaF and Gpp(NH)p, the enhancement of [3H]-forskolin binding did not differ between control and the drug treated groups. 6. Chronic (--)-tertatolol or (--)-propranolol treatment therefore did not produce an increase in receptors in heart, lung or skin but the beta-adrenoceptor-mediated responses were enhanced. In addition, [3H]-forskolin binding did not increase suggesting that the hypersensitivity was not due to changes in the number of receptors or adenylate cyclase. Hypersensitivity following beta-adrenoreceptor antagonist administration may therefore involve enhanced coupling of receptors to G-proteins.

Adrenergic beta-Agonists↗
PubMed1970

Comparison of the effects of propranolol and MJ 1999 on cardiac beta-adrenoceptors in man.

1. Propranolol, a beta-adrenoceptor blocking drug with local anaesthetic and a direct myocardial depressant action, and MJ 1999, a beta-adrenoceptor blocking drug which has no local anaesthetic or intrinsic sympathomimetic action, were compared for beta-adrenoceptor blocking activity in man.2. Propranolol was 2.67 times more active than MJ 1999 in reducing by 50% the tachycardia produced by the intravenous infusion of isoprenaline in healthy volunteers.3. Propranolol and MJ 1999 intravenously both reduced resting heart rate in the standing position and an exercise tachycardia, but there was no qualitative or quantitative difference between them.4. On oral administration, both propranolol and MJ 1999 reduced resting heart rate and an exercise induced tachycardia; propranolol was only slightly more active than MJ 1999.5. In patients with thyrotoxicosis propranolol was about twice as active as MJ 1999 in reducing the heart rate.

Adrenergic beta-Antagonists↗
PubMed1974

Effects of tiprenolol, practolol and propranolol on experimental ventricular tachyarrhythmias.

1 Low doses of tiprenolol (0.01-0.02 mg/kg) and propranolol (0.05 mg/kg) abolished the ventricular arrhythmias produced by the intravenous injection of adrenaline in anaesthetized dogs respired with halothane.2 Larger doses of tiprenolol (2.0-4.0 mg/kg) restored sinus rhythm in four of five dogs with ventricular tachycardia produced by toxic doses of ouabain. Propranolol (2.0-4.0 mg/kg) had the same effect in each of four dogs.3 Both tiprenolol (4.0-8.0 mg/kg) and propranolol (4.0 mg/kg) increased the frequency of sinus beats and reduced the ventricular rate in dogs with ventricular tachycardia 20-44 h after ligation of a coronary artery.4 Practolol (0.5-16.0 mg/kg) did not reduce the ventricular rate or increase the frequency of sinus beats in dogs with ventricular tachycardia after ligation of a coronary artery.5 In dogs with ouabain-induced ventricular tachycardia mean arterial pressure was reduced after the administration of tiprenolol (0.5-8.0 mg/kg) or propranolol (4.0-8.0 mg/kg). Depression of sinus and atrioventricular nodal function, and of intraventricular conduction developed in some of the dogs given tiprenolol (4-8 mg/kg) or propranolol (8.0 mg/kg).6 The administration of tiprenolol (1.0-8.0 mg/kg) or propranolol (4.0-8.0 mg/kg) depressed the arterial pressure and caused the deaths of some dogs in which a coronary artery had been ligated. Such deaths did not occur in the group which had been given toxic doses of ouabain.

Adrenergic beta-Antagonists↗
PubMed1976

Antioxotremorine action of propranolol.

1. The influence of propranolol on the neuromuscular, tremor-producing and muscarinic effects of oxotremorine was examined. 2. In the isolated rat phrenic nerve-diaphragm preparation the neuromuscular blocking effect of oxotremorine was inhibited by propranolol in a dose-dependent manner. 3. Propranolol intensified the paralytic effect of tubocurarine in the rat diaphragm and prevented antagonism of tubocurarine paralysis by tetraethylammonium. 4. Propranolol was devoid of any curare-like effect in the isolated rectus abdominis muscle of the frog. 5. Vasodepressor responses to oxotremorine in rats and spasmogenic responses to oxotremorine in guinea-pig ileum were not antagonized by propranolol. 6. A dose-dependent antagonism of oxotremorine-induced tremor in mice was observed after pretreatment with propranolol and it is suggested that this effect is due to an antagonism of a presynaptic effect of oxotremorine at skeletal neuromuscular junctions.

Animals↗
PubMed1976

Comparative effects of propranolol and practolol in the early stages of experimental canine myocardial infarction.

1 The effects of propranolol and practolol, at equivalent myocardial beta-adrenoceptor blocking doses, (as assessed by the degree of shift of isoprenaline dose-response curves) were investigated in anaesthetized greyhounds before and after acute coronary artery ligation. 2 When administered intravenously to the intact close-chest dog, propranolol (0.1 mg/kg) and practolol (0.5 mg/kg) caused similar decreases in heart rate, left ventricular dP/dt max, myocardial blood flow and cardiac output. Only propranolol increased peripheral vascular resistance. 3 When administered 2-3h after acute coronary artery ligation, propranolol (0.1 mg/kg) significantly decreased blood flow in both normally perfused and ischaemic regions of the heart. There was also electrocardiographic evidence of further deterioration after propranolol; two out of seven animals died following this treatment. 4 Practolol (0.5 mg/kg) when administered after coronary artery ligation also decreased normal myocardial blood flow but flow in the ischaemic area remained unchanged. Evidence was obtained from electrocardiographic, myocardial temperature, myocardial O2 consumption and lactate measurements that the administration of practolol, in contrast to propranolol, benefited the ischaemic myocardium. 5 Analysis of the results suggests that this beneficial action of practolol may be related to at least two mechanisms. Firstly the ability of practolol to increase the period during diastole when perfusion of the subendocardium is possible, without decreasing the transventricular pressure during this period. Secondly that practolol does not unmask alpha-adrenoceptor vasoconstriction in the ischaemic region.

Animals↗
PubMed1980

Curare-like effect of propranolol on rat extraocular muscles.

1 The effects were studied of the beta-adrenoceptor blocking drug, (+/-)-propranolol and its (+)- and (-)-isomers on contractility of rat isolated diaphragm and inferior rectus muscles. 2 Propranolol (10(-5) M) did not modify the resting tension nor the electrically-induced twitch contraction in diaphragm and extraocular muscles, nor the tonic tension evoked in the latter by high K concentrations. 3 In inferior rectus preparations (+/-)-propranolol (5 x 10(-6) M) reduced significantly tensions evoked by succinylcholine (SCh). Cumulative dose-response curves to SCh were shifted to the right in a nearly parallel manner by (+)- and (-)-propranolol which were about equiactive. 4 It is concluded that the depressant action of propranolol is independent of its adrenoceptor blocking potency and it is not due to an alteration of the contraction mechanism. Propranolol appears to depress SCh-evoked tensions through a curare-like effect on cholinoceptors.

Animals↗
PubMed1981

Inhibition of lymphocyte capping and transformation by propranolol and related compounds.

1 The effects of propranolol on phytohaemagglutinin (PHA)-induced transformation of murine T lymphocytes and capping of anti-IgG on the surface of murine B lymphocytes have been examined. 2 A 50% inhibition of transformation was observed with 10(-5) M propranolol, whereas a higher concentration, of the order of 10(-3) M propranolol was required to inhibit capping by 50%. The (+)-and (-)-isomers of propranolol proved equipotent in these respects, and the relative potencies of selected analogues of propranolol (alprenolol, oxprenolol, metoprolol, practolol, and sotalol) coincided with their potencies as membrane stabilizers; however, lymphocyte transformation was consistently more sensitive than capping. 3 Similar effects were also seen with quinidine, chlorpromazine and lignocaine, and it was concluded that the inhibition of both lymphocyte functions was due to the membrane stabilizing actions of propranolol.

Adrenergic beta-Antagonists↗
PubMed1981

Comparative studies of (--)-, (+/-)-propranolol, atenolol, guanethidine, bretylium and tetracaine on adrenergic transmission.

1 Effects of (--)-, (+/-)-, and (+)-propranolol, atenolol, guanethidine, bretylium and tetracaine were studied on relaxation responses of rabbit ileum and contractile responses of rabbit pulmonary artery and guinea-pig vas deferens to electrical nerve stimulation (2 to 50 Hz). 2 In the ileum, inhibition by tetracaine 3.3 x 10(-6) M occurred at high frequencies of stimulation, while bretylium 1.2 x 10(-4) M and guanethidine 2 x 10(-5) M inhibited responses at all frequencies, the latter producing greater inhibition at low frequencies. 3 (+/-)-Propranolol 10(-5) M produced a tetracaine-type inhibition after 1 h and a bretylium-pattern after 2 h in the ilea and pulmonary arteries and a transition from bretylium- to guanethidine-pattern in the vas deferens, while atenolol 2 x 10(-5) to 10(-4) M produced guanethidine-type inhibition in all preparations. 4 (--)-, (+/-)-, and (+)-Propranolol 3 x 10(-6) to 3.3 x 10(-5) M were equipotent in the vas deferens and ileum. However, inhibition by (--)-propranolol 3.3 x 10(-5) M persisted in the ileum, while that by the (+)-isomer was partially restored by washing. 5 (--)- or (+)-Propranolol 3.3 x 10(-5) M or atenolol 2 x 10(-5) M did not inhibit relaxation of the ileum after the bath temperature was maintained at 4 degrees C for 2 h during drug application. 6 In conclusion, propranolol and atenolol both have gradually developing guanethidine-like adrenergic neurone blocking actions.

Animals↗
PubMed1981

The action of propranolol on factors concerned with the delivery of oxygen to the tissues.

1 In a previous study in conscious rats, orally administered propranolol acutely lowered cardiac output by 30.5% and oxygen uptake by 12.2%, while oxygen extraction rose by 31.5%. The present study is concerned with the way in which the rat meets its oxygen requirements against such a fall in perfusion. 2 The effect of known concentrations of propranolol on haemoglobin-oxygen affinity was studied in vitro. The effect of orally administered propranolol (given acutely and chronically) was then determined and this was related to the concentration of the drug in plasma and red cells. Further studies were made on the action of propranolol on the Bohr effect and on arterial oxygen carriage. 3 In vitro, high concentrations of propranolol (1 x 10(-4) M) influenced haemoglobin-oxygen affinity in a biphasic manner and this was associated with changes in haematocrit and red cell and plasma pH. No change occurred in affinity after acute or chronic oral administration of the drug due to insufficient concentration in the blood. No direct action of the Bohr effect was detected. 4 Arterial oxygen content rose acutely due to an increase in haemoglobin concentration. 5 It is concluded that increased oxygen extraction in propranolol-treated rats is not explained by the actions of the drug on haemoglobin-oxygen affinity.

Animals↗
PubMed1984

Anti-arrhythmic effects of prazosin and propranolol during coronary artery occlusion and re-perfusion in dogs and pigs.

Open-chest dogs and pigs anaesthetized with pentobarbitone were used to evaluate the anti-arrhythmic effect of prazosin and propranolol during a 30 min period of occlusion of the left anterior descending coronary artery followed by 15 min of re-perfusion. In dogs, both prazosin and propranolol reduced the incidence of ventricular premature depolarizations and ventricular tachycardia during the occlusion period. During the 45 min period of occlusion and re-perfusion, the incidence of ventricular fibrillation was significantly reduced in the prazosin-treated and propranolol-treated dogs. In pigs prazosin reduced the incidence of ventricular premature depolarizations during occlusion and propranolol reduced the incidence of both ventricular premature depolarizations and ventricular tachycardia during occlusion, but the incidence of ventricular fibrillation was not significantly reduced in the prazosin- and propranolol-treated pigs. Prazosin reduced arterial pressure and propranolol lowered heart rate in both dogs and pigs, but a comparison of mean arterial pressure and heart rate in animals surviving and those not surviving the 30 min of coronary artery occlusion and 15 min of re-perfusion showed no significant difference.

Animals↗
PubMed1987

Inhibition of adrenomedullary catecholamine release by propranolol isomers and clonidine involving mechanisms unrelated to adrenoceptors.

1 Transmural electrical stimulation (10 Hz, 40 V, 1 ms for 60s) increased total catecholamine secretion from perfused cat adrenal glands; this response was enhanced by neostigmine and inhibited by mecamylamine, suggesting that release of acetylcholine from splanchnic nerve terminals was stimulating nicotinic receptors and enhancing catecholamine secretion. 2 Isoprenaline, (-)-propranolol and (+)-propranolol (10(-7)-10(-5)M) inhibited the electrically-evoked secretory response by 40-70%; similar reductions were obtained with clonidine and yohimbine. Neither, (+)-propranolol nor (-)-propranolol inhibited K-evoked secretion from cat adrenals; in contrast, nimodipine potently inhibited it (IC50 = 24 nM). 3 Either, racemic propranolol or the (+)- or (-)-isomers (1-10 microM) equally inhibited [3H]-noradrenaline release evoked by nicotine or acetylcholine from cultured bovine adrenal chromaffin cells; clonidine (10 microM) inhibited secretion by 50% and yohimbine or isoprenaline did not affect it. 4 The results indicate that adrenomedullary catecholamine release evoked by splanchnic nerve stimulation is not modulated by alpha- or beta-adrenoceptors and suggest that propranolol may inhibit secretion by blocking ion fluxes through the acetylcholine receptor ionophore. Clonidine may inhibit secretion by this same mechanism, and/or by interfering with some intracellular event in the secretory mechanism.

Adrenal Medulla↗
PubMed1994

Pharmacological actions of the selective and non-selective beta-adrenoceptor antagonists celiprolol, bisoprolol and propranolol on human bronchi.

1. The pharmacological actions of the beta-adrenoceptor antagonists, celiprolol, bisoprolol and propranolol were investigated in human lung tissue by radioligand binding experiments as well as in human isolated bronchi by functional experiments in organ baths. 2. Data from lung tissue were compared to those obtained from myocardial membranes. 3. Lung tissue was obtained from 10 patients having undergone lung resection for bronchial carcinoma and myocardial tissue from a patient who had received a heart transplantation. 4. In radioligand binding experiments, celiprolol exhibited a high affinity binding to beta 1-adrenoceptors in heart and a low affinity binding to beta 2-adrenoceptors in lung tissue. The selectivity obtained for the beta 1-adrenoceptor was calculated to a factor of eleven. 5. Compared to bisoprolol and propranolol, celiprolol elicited the lowest affinity for the beta-adrenoceptor, as judged from the K1-values. 6. In the absence and presence of the guanine nucleotide Gpp(NH)p celiprolol did not affect receptor binding. 7. In functional experiments on intact bronchi, celiprolol, bisoprolol and propranolol failed to produce relaxation (+/- forskolin) or a significant difference in efficacy in antagonizing the relaxant effects of isoprenaline. However, a rank order of potencies was revealed (propranolol:bisoprolol:celiprolol = 46:12:1). 8. Plasma concentrations for celiprolol and bisoprolol usually achieved in vivo were below the IC50 value obtained in vitro. In contrast, for propranolol, plasma concentrations were nearly identical with the IC50 value. 9. It is concluded that celiprolol is a selective beta 1-adrenoceptor antagonist on human heart and has no agonistic properties on intact human bronchi. Compounds such as celiprolol and bisoprolol may in comparison to propranolol, possess reasonable therapeutic advantages in the treatment of patients with obstructive lung disease due to their low affinity for beta 2-adrenoceptors.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1995

Alteration of ventricular fibrillation by propranolol and isoproterenol detected by epicardial mapping with 506 electrodes.

INTRODUCTION: We hypothesized that drugs which alter ventricular refractoriness or excitability produce quantifiable changes in ventricular fibrillation. METHODS AND RESULTS: We used a 528-channel mapping system to quantify the effects of the beta-antagonist, propranolol, and the beta-agonist, isoproterenol, on activation patterns in ventricular fibrillation. A plaque of 506 (22 x 23) electrodes spaced 1.12 mm apart and covering about 5% of the ventricular epicardium was sewn to the anterior right ventricle in 18 pigs (30 kg). Propranolol (0.25 to 0.4 mg/kg) increased the refractory period at a right ventricular epicardial site while isoproterenol (3 to 5 micrograms/min) shortened it. Ventricular fibrillation was induced by programmed stimulation, and unipolar electrograms were recorded from the 506 plaque electrodes for 2 seconds beginning 1, 15, and 30 seconds after the onset of fibrillation. Active epicardial recording sites were identified from the first derivative of the unipolar potentials (dV/dt) detected at each electrode. Then, neighboring active sites were grouped into activation fronts by computer analysis. In six pigs the effect of repeated inductions of ventricular fibrillation was assessed by comparing ventricular fibrillation after saline with a preceding control episode of fibrillation. Each activation front excited 40% +/- 46% of the mapped region before blocking. No changes were observed with saline and multiple inductions of fibrillation. In another six pigs, ventricular fibrillation after propranolol was compared with a preceding control episode of fibrillation. Ventricular fibrillation after propranolol exhibited a decreased activation rate per epicardial recording site and fewer activation fronts per second. There was no change in the amount of tissue excited by each activation front or the number of reentry cycles per activation front compared with control. In addition, there was no change in the maximum negative dV/dt detected per activation at an epicardial site. In six pigs ventricular fibrillation during isoproterenol was compared with control episodes of ventricular fibrillation before and 45 minutes after washout of the drug. The control episodes of fibrillation were not different from each other. Compared with control, ventricular fibrillation during isoproterenol exhibited an increased activation rate per epicardial site, an increased amount of tissue excited by each activation front, and an increased maximum negative dV/dt for each activation. There was no change in the number of activation fronts per second or the number of reentry cycles per activation front compared with control. CONCLUSION: Quantitative analysis revealed that propranolol and isoproterenol do not have symmetrically opposite effects on ventricular fibrillation. Propranolol decreased the number of activation fronts while isoproterenol increased the amount of tissue excited by each activation front. Thus, drugs that alter ventricular refractoriness or excitability alter ventricular fibrillation.

Animals↗
PubMed1997

Influence of epinephrine, propranolol, and atrial pacing on spatial distribution of recovery time measured by body surface mapping in congenital long QT syndrome.

INTRODUCTION: Sympathetic stimulation plays an important role in the genesis of QT(U) prolongation and ventricular arrhythmias in congenital long QT syndrome (LQTS). Permanent pacemaker as well as beta blockers are reported to be effective in the management of this syndrome. The purpose of this study was to examine influence of epinephrine (alpha- and beta-adrenergic stimulation), propranolol (beta blocker), and atrial pacing on the spatial distribution of repolarization using body surface recovery time (RT) in congenital LQTS. METHODS AND RESULTS: Body surface mapping was recorded in 16 patients with congenital LQTS and 20 control patients before and after epinephrine infusion (0.1 microg/kg per min), oral propranolol (1 to 2 mg/kg per day), addition of epinephrine during oral propranolol, atrial pacing at a cycle length of 600 or 750 msec, and addition of epinephrine during atrial pacing. The RT, that is, the interval between the QRS onset and the maximum dV/dt point in the ST-T segment, was measured automatically by a computer from each of the 87 mapping leads, and the corrected RT (RTc) was calculated using Bazett's method. In patients with congenital LQTS, epinephrine markedly changed the T(U) wave morphology and spatial distribution of RT, especially the distribution of maximum RT of the left anterior chest and back. Epinephrine prolonged the maximum RTc and the minimum RTc in 87 leads and increased the RTc dispersion (difference between maximum and minimum RTc in each patient). Neither propranolol nor atrial pacing changed the T(U) wave morphology, spatial distribution of RT, or any RTc parameters at rest. Propranolol prevented the influences of epinephrine on the T(U) wave morphology, spatial distribution of RT, and RTc parameters, whereas atrial pacing did not. In control patients, marked changes of the T(U) wave morphology and RTc parameters were not recognized during the entire protocol. CONCLUSIONS: Our results indicate that epinephrine markedly changes the spatial distribution of repolarization and increases the dispersion of repolarization, which probably are linked to arrhythmogenesis in congenital LQTS. The data suggest that propranolol but not atrial pacing are effective to suppress repolarization abnormalities during sympathetic stimulation.

Adolescent↗