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At least 955 records · Page 53Linked to original sources
PubMedDate not supplied

Involvement of Central adrenergic mechanisms in the induction of cardiac arrhythmias by aconitine nitrate administered intraventricularly.

Aconitine, 10 mug, administered intraventricularly in cats produced cardiae arrhythmias. Intraventricular administration of phenoxybenzamine, propranolol and practolol abolishes the centrally induced cardiac arrhythmias. Intraventricular reserpinization also abolished these cardiac arrhythmias whereas intraventricular administration of 6-hydroxydopamine and tetrabenazine had no effect. Brain stem noradrenaline probably plays a role in these centrally induced cardiac arrhythmias by aconitine.

Aconitine↗
PubMed1975

Phaeochromocytoma in childhood. A case report.

The clinical features of a 9-year-old boy with an extra-adrenal phaeochromocytoma, complicated by malignant hypertension, are described. The value of urinary and blood catecholamine assays and specialised radiological investigations in the accurate localisation of the tumour, is emphasised. Successful removal of the tumour was facilitated by pre-operative control of the hypertension with a combination of alpha and beta-adrenergic blockade (phenoxybenzamine and practolol). Intra-operative control of fluctuations in blood pressure was simplified by the use of Ethrane (enflurane compound 347) as one of the anaesthetic agents. As a result, sodium nitroprusside was infrequently used.

Anesthesia, General↗
PubMed1976

Effect of adrenergic blockade on gastric secretion altered by catecholamines in rats.

The effect of adrenergic blockade on gastric secretion altered by catecholamines was studied for 4 hr after injection in rats with chronic gastric fistulas. The alpha-adrenergic blockers phenoxybenzamine and phentolamine significantly inhibited the basal secretion of HCl and pepsin. Blockade of the beta-adrenergic receptors with propranolol did not change this secretion. Practolol in small doses slightly increased and in larger doses inhibited HCl out-put. Of the catecholamines, adrenaline and dopamine most markedly reduced HCl and pepsin secretion, while noradrenaline and isoprenaline had a weaker effect. Neither alpha- nor beta-adrenergic blockers prevented the inhibitory action of the catecholamines employed, but intensified the depression of the gastric secretion provoked by them. Adrenergic blockers inhibited secretion after catecholamines as well as basal secretion. This indicates that these two antagonistic groups of compounds act independently on the mechanism controlling gastric secretion. It is unlikely that this takes place indirectly through changes in the blood supply of the gastric mucosa.

Adrenergic alpha-Antagonists↗
PubMed1975

Role of sympathetic excitation in generating arrhythmias in early and late phases of ectopic responses after coronary arterial occlusion in dog heart.

The three phases of arrhythmias that develop within specific durations of occlusion of a coronary artery of the dog have been reviewed and characterized. The intravenous administration of practolol as described has virtually prevented the occurrence of arrhythmic activity during the first 7-8 hr after occlusion and kept the frequency at a much reduced level as compared with controls through 10 or 11 hr, but not appreciably longer. This means that first and second phase arrhythmias were almost abolished, and development of third phase ventricular tachycardia was significantly retarded, but not prevented. It is concluded that sympathetic stimulation is an important component in the effective excitation of ectopic activity during the first and second phases, but contributed no more than a minor component to the fully developed third phase activity.

Animals↗
PubMed1975

Influence of the adrenal medulla on cardiac rhythm disturbances following acute coronary artery occlusions.

The present study was designed to examine the relationship between epinephrine secreted from the adrenal medulla and acute occlusion of the left anterior descending (LAD) coronary artery in alpha-chloralone-anesthetized cats. Occlusion of the LAD artery produced arrhythmia in all of the animals, with 39% developing ventricular fibrillation (VF). Epinephrine content in the adrenal venous blood increased 5-fold immediately after occlusion and was associated with the development of arrhythmia and VF. The adrenal venous epinephrine levels increased 8-fold after occlusion in the animals that developed VF while, in those that did not develop VF, the epinephrine levels increased only 1.5-fold. Bilateral ligation of the adrenal veins 1 hour prior to occlusion of the LAD artery did not alter the pattern of development of arrhythmia but prevented the occurrence of VF. Pretreatment of animals with either practolol or sotalol 15 min prior to LAD artery occlusion also did not affect the occurrence of arrhythmia but prevented the incidence of VF. The data indicate that acute occlusion of the LAD coronary artery produces a sharp rise in epinephrine from the adrenal medulla and that epinephrine is a major factor in producing VF but does not seem to be involved to any great extent in the production of less ominous ventricular arrhythmias.

Adrenal Medulla↗
PubMed1975

Positive inotropic action of insulin on piglet heart.

This study was designed to investigate changes in cardiac performance during hypoglycemia produced by the administration of insulin in the newborn piglet. With heart rate, aortic pressure, and aortic flow held constant, the treated group demonstrated a pronounced positive inotropic response manifested by an increase of dP/dt max to 138% of control values. Central nervous system function and beta adrenergic activity were excluded from the preparation by ligation of the brachiocephalic vessels and administration of practolol. For reasons discussed, it is unlikely that the findings can be ascribed to glucagon contamination. Therefore, the increase in contractility presumably resulted from a direct effect of insulin upon the myocardium. Clinical and laboratory data suggest that the resistance of the neonate to hypoxia is modified by glycogen stores. Insulin is known to increase glycogen synthesis, and this effect might be expected to augment myocardial resistance to hypoxia. Under the conditions of these experiments, however, pretreatment with insulin had no demonstrable influence on the rate of deterioration of cardiac function during hypoxia. The mechanism of cardiac stimulation by insulin is unknown but may involve calcium fluxes.

Animals↗
PubMed1975

Myocardial high energy phosphates in experimental thyrotoxicosis in guinea pigs.

Experimental thyrotoxicosis was produced in guinea pigs by daily intraperitoneal injection of 0.7 mg/kg thyroxine (T4) or 0.15 mg/kg triiodothyronine (T3), as shown by an increase of PBI over 50 gamma percent, weight reduction of 20--30 percent, and increase in heart rate of 30--50 percent. Control animals received solvent only. Metabolites were determined in heart muscle on the 1st, 3rd, and 7th day using freeze-stop technique and enzymatic methods: creatine phosphate (CP), ATP, ADP, AMP, glucose 6-phosphate (G-6-P), fructose diphosphate (FDP), pyruvate, lactate, and inorganic phosphate (Pi). In thyrotoxic animals there was a decrease in CP which became significant after 3 days and more pronounced after 7 days. The ratio of CP to Pi decreased. G-6-P and FDP levels increased. The results were identical after administration of T4 and T3. ATP decreased slightly and ADP increased slightly after T4. Propranolol up to a dose of 3 mg/kg or practolol up to 10 mg/kg given daily i.p. on the 4th to 7th day did not prevent either the T4-induced decrease in high energy phosphates or the increase in G-6-P.

Adenine Nucleotides↗
PubMed1976

Effect of autonomic blockers on the heart rate of intact rats and animals with artificial hyperthyroidism.

The effect of various autonomic blockers on the heart rate (from the ECG recording) of intact rats and of animals with experimental hyperthyroidism induced by the administration of dried thyroid was studied. In intact rats, the heart rate fell significantly (by 22%) during the first week after the peroral administration of propranolol (0.05% in food), but trimepranol (0.02%), reserpine (0.001%) and guanethidine (0.1%) had no effect (in a suplementary experment, a small, but statistically significant decrease was also found after trimepranol). In experimental hyperthyroidism, using the same blocker doses, the heart rate fell significantly after propranolol (by 23%), trimepranol (22%), reserpine (16%) and, in a preliminary experiment, guanethidine (19%). On injecting 0.05 mg propranolol intravenously, the maximum drop in the heart rate in intact rats was 22%, while in hyperthyroidism it was hardly more than half this value (at all the intervals from 2 to 30 minutes the decrease was statistically significant). Practolol, in a dose of 0.3 mg i.v., was less effective -- in intact rats the heart rate fell by not more than 12% (at all the intervals from 2 to 30 minutes the decrease was significant), but in hyperthyroidism the drop was slower and statistically non-significant. The results do not furnish an unequivocal answer to the question of the role of adrenergic regulation of the heart rate under physiological conditions and in experimental hyperthyroidism in rats.

Animals↗
PubMedDate not supplied

[Toxicologic analysis of some adrenergic-beta blockers in the diagnosis of intoxications].

The study aimed at finding effective techniques of qualitative and quantitative analysis of selected beta-adrenergic blockers, useful both for monitoring of therapy and for thanatological diagnosis of intoxications. The studies took advantage of gas chromatography (GLC) and high performance liquid chromatography (HPLC). For isolation of studied compounds from biological material, classical and solid phase extraction procedures (SPE) Extrelut-20 (Merck), Abselut Nexus (Varian), STRATA C--18 E (Phenomenex) were used. The program included the analysis of most frequently applied derivatives: Acebutolol, Atenolol, Bunitrolol, Bupranolol, Labetolol, Metipranolol, Metoprolol, Oxprenolol, Practolol, Propranolol.

Acebutolol↗
PubMed1977

Differential inhibition of lipolysis in human adipose tissue by adrenergic beta receptor blocking drugs.

The effects of various adrenergic beta receptor agonists and antagonists on lipolysis (measured as glycerol release) in human adipose tissue in vitro were studied. Of the agonists investigated, the potency rank order was isoproteronol greater than norepinephrine greater than salbutamol. Adrenergic beta receptor blocking drugs inhibited catecholamineinduced lipolysis competitively. Propranolol was the overall most effective compound, followed by metoprolol, alprenolol and practolol, whereas butoxamine and H35/25 were weak inhibitors. The results indicate that the adrenergic reciptor mediating lipolysis in human adipose tissue is of type beta-1. Basal and theophylline-induced lipolysis was reduced when higher concentrations of these drug were used.

Adipose Tissue↗
PubMed1977

Specific enhancement of norepinephrine-induced contraction in rat veins after beta adrenergic antagonists.

Propranolol markedly increased the norepinephrine-induced maximal force in circular smooth muscle of the rat portal, mesenteric, renal and, to a lesser extent, femoral veins without affecting aortic or mesenteric artery responses to norepinephrine. Furthermore, two other beta receptor antagonists, practolol and N-isopropylmethoxamine, specifically enhanced maximal venous responses to norepinephrine. Contractions to norepinephrine, but not to serotonin, were increased by propranolol only in veins, even after the vasodilator, papaverine. The ability of propranolol to enhance norepinephrine-induced contraction in these rat veins paralleled the effectiveness of isoproterenol to relax such tissues. In addition, beta receptor antagonists enhanced the response of veins to the field stimulated release of norepinephrine from sympathetic nerves. These data support the conclusion that beta adrenergic stimulation modulates norepinephrine-induced constriction in certain rat veins but not in the aorta or mesenteric artery.

Adrenergic beta-Antagonists↗
PubMed1975

D-Thyroxine in hyperbetalipoproteinaemia.

D-Thyroxine was administered intermittently to 11 patients with hyperlipoproteinaemia (Fredrickson type lla). To avoid possible untoward cardiac stimulation, practolol was prescribed with it. Cholesterol levels were measured regularly over a period of 4 years. A temporary drop of about 15% in the mean cholesterol level was obtained. It is, however, concluded that the over-all response is unimpressive.

Adult↗
PubMed1977

Effect of beta adrenergic blocking drugs on the renin-aldosterone system, sodium excretion, and renal hemodynamics in cirrhosis with ascites.

As a result of effective beta adrenergic blockade with either propranolol or practolol, plasma renin activity was suppressed in all of 11 patients with cirrhosis and ascites. In contrast, the effect on the rate of renal excretion of aldosterone was variable, suggesting that factors other than the renin-angiotension system are responsible for the control of aldosterone secretion in cirrhosis. The changes in aldosterone could not be explained on the basis of changes in the plasma concentrations of potassium or sodium. The renal sodium excretion was inversely related to the values for aldosterone both before and after beta adrenergic blockade, indicating a major role for aldosterone in regulating sodium excretion. A number of patients had an abnormal intrarenal distribution of plasma flow with a relative hypoperfusion of the renin-secreting outer cortical nephrons. Plasma renin activity was inversely related to outer cortical plasma flow, suggesting that the reduced outer cortical flow may be a stimulus to increased renin secretion. Because the abnormal intrarenal hemodynamic pattern was not corrected by suppression of plasma renin activity, and presumably angiotension II concentrations, it is unlikely that it is attributable to the known renal vasonconstrictor effects of angiotensin II.

Adrenergic beta-Antagonists↗
PubMed1990

Adrenergic dependence of the platelet aggregation in rats.

The paper examines the effect of different adrenergic agents influencing both the neuronal unit of the adrenergic transmitter system and its alpha- and beta-receptor components on the ADP-induced platelet aggregation. A considerable inhibition of the platelet aggregation is found under conditions of post-reserpine adrenergic block (16.06%, p less than 0.001) and blocking of the beta 1-adrenergic receptors with practolol, applied independently (45.06%, p less than 0.001) and prior to the treatment of the rats with dobutamine--beta 1-adrenoreceptor agonist (52.20%, p less than 0.001). The stimulation of these receptors with dobutamine accelerates the platelet aggregation by 41.04% (p less than 0.001). No changes in the platelet aggregation are found after treatment with phenoxybenzamine (nonselective alpha adrenergic blocker) and salbutamol (beta 2-adrenergic agonist). It may be concluded that the ADP-induced platelet aggregation depends to a certain extent on the functional state of the neuronal and beta-adrenoreceptor unit of the adrenergic transmitter system and possibly also on the metabolic processes connected with them.

Adenosine Diphosphate↗
PubMed1990

Pharmacological evaluation of new alkylesters of 4-[(2-hydroxy-3-alkylamino)propoxy]phenylcarbamic acids with beta-adrenolytic properties.

The basic relationship between the chemical structure and pharmacological activities of new alkylesters of 4-[(2-hydroxy-3-alkylamino)propoxy]phenylcarbamic acids were evaluated. The efficiency of compounds was compared with those of metipranolol and practolol, respectively. The majority of 4-substituted derivatives of aryloxypropanolamines have shown antiisoprenaline (beta-adrenolytic) and local anesthetic (membrane stabilizing) activities. The values of LD50 and/or partition coefficients have not differed significantly when compared with those of standard metipranolol.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

cAMP activity and isoproterenol-induced myocardial injury in rats.

Isoproterenol-induced myocardial necrosis (ISO-MN) was obviated by the cardioselective beta-blocker, practolol, suggesting that ISO-MN is caused by specific activation of myocardial beta-adrenergic receptors. Because cAMP is the "second messenger" in such activation, enhanced activity of cAMP should aggravate ISO-MN. Pretreatment of rats with bretylium in various amounts, elicited no ill effects but enhanced the effects of ISO on the cAMP activity and also intensified the ISO-induced structural changes in the myocardium.

Animals↗
PubMedDate not supplied

The effect of beta-adrenergic receptor blocking agents on hypertensive action of noradrenaline injected into the lateral ventricle of rat brain.

Noradrenaline (NA), 100 microgram intraventricularly (ivtr), produces an evident hypertension, lasting for up to 15 min. A previous ivtr administration of propranolol (100 and 500 microgram), alprenolol (100 microgram), sotalol (100 microgram), (-)INPEA (100 microgram), (+)INPEA (100 microgram), Ko 1366 (100 and 200 microgram), or practolol (20 microgram) abolishes the hypertensive action of NA. The results indicate that the central nervous system of the rat contains structures similar to the peripheral beta-adrenoceptor, and that they are involved in the central regulation of circulation.

Adrenergic beta-Antagonists↗
PubMed1977

Comparative study of beta andreoceptor antagonists on the isolated atria of control and of the reserpine treated rabbits.

The effect of four adrenoceptor antagonists, chosen because of reported differences in their selectivities, were compared using the positive chronotropic response to isoprenaline on isolated rabbit atria. Oxprenolol was the most potent antagonist of the isoprenaline induced cardiac arrhythmias. Alprenolol, practolol and propranolol also blocked the positive chronotropic responses to isoprenaline effectively. All the antagonists lowered the resting heart rate. The effects of all four selected antagonists on heart rate probably result from cardiac beta adrenoceptor blockade. Atria isolated from reserpine treated rabbits, showed a reduced percentage of increase in the heart rate in response to addition of isoprenaline. This decreased response has been related in some cases to direct myocardial inhibition.

Adrenergic beta-Antagonists↗