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PubMed1980

[Pemphigus and pemphigoid].

This comparison of the two diseases--pemphigus and pemphigoid--aimed particularly on points of actual interest. Are thus reviewed: (1) the research on the influence of racial or genetic factors in pemphigus vulgaris; (2) the striking differences between the immunological criteria of the two; (3) the clinical polymorphism of pemphigus: besides pemphigus superficialis, non-bullous forms, usually milder, of various types: herpetiformis, circinate ... are now being described; (4) the importance in all cases of eosinophilic spongiosis; (5) the clinical monomorphism of classical bullous pemphigus; on the contrary, the differences, both from clinical and prognostic points of view, in localized bullous pemphigoid (from the benign mucocutaneous form to the severe scarring disease) and in bullous pemphigoid of children; (3) the cases of genuine pemphigus induced by drugs (D-penicillamine, rifampicine) and the problem of the pemphigus-like antibodies; (7) bullous pemphigoid, UV light and practolol; (8) the outstanding association of two major immune diseases, pemphigus vulgaris, myasthenia and thymoma; (9) the mixed bullous dermatoses: pemphigus vulgaris and dermatosis herpetiformis (to separate from herpetiform pemphigus), bullous pemphigoid and dermatosis herpetiformis (bringing up the unsolved problem of mixed or intermediate forms of the two diseases), bullous pemphigoid and pemphigus vulgaris, exceptionally seen, and (10) some news on therapy.

Adult↗
PubMed1980

[D-penicillamine-induced pemphigus].

The authors describe a new original observation of a D-penicillamine-induced pemphigus in a patient with rheumatoid polyarthritis. It begins in two steps: the first crisis of blisters having subsided after withdrawal of D-penicillamine, there is a recurrence 7 months later. Clinical and histopathological aspects of pemphigus vulgaris are discussed. Existence of intercellular antisubstance antibody in the serum and in the skin. Evolution identical to that of a classical pemphigus requiring an important corticotherapy. Review of the literature on the previous cases of D-penicillamine-induced pemphigus and other pemphigus attributed to the action of other drugs, namely pyritinol, rifampicine and practolol. Discussion of the pathogenesis.

Arthritis, Rheumatoid↗
PubMed1980

Protection against adrenochrome-induced myocardial damage by various pharmacological interventions.

Perfusion of the isolated rat heart with Krebs-Henseleit solution containing adrenochrome (25 or 50 mg/l), and oxidation product of catechalmines, resulted in contractile failure and myocardial necrosis. Various pharmacological agents known to protect the myocardium against catecholamine-induced necrosis were also found to be effective against adrenochrome-induced changes in the ultrastructure of the isolated perfused rat heart. The alpha-receptor-blocking drugs tolazoline and Dibenamine (dibenzylchlorethamine), and the adrenergic neurone-blocking agents guanethidine and bretylium did not alter the development of contractile failure and necrosis due to adrenochrome. The beta-receptor-blocking compounds propranolol and practolol effectively protected the heart from adrenochrome-induced necrotic damage, and partially prevented contractile failure. The hydrazine-type monoamine oxidase inhibitor iproniazid completely prevented ultrastructural damage and partially maintained contractile-force development in adrenochrome perfused hearts. The non-hydrazine-type monoamine oxidase inhibitor tranylcypromine partially protected the isolated rat heart against adrenochrome necrosis, but disruption of mitochondrial structure was still seen. Tranylcypromine did not significantly improve contractile force development during adrenochrome perfusion. The calcium antagonist D-600 reduced the severity of adrenochrome-induced ultrastructural damage. These results provide strong support for the view that catecholamine-induced cardiotoxicity is mediated through the formation of adrenochrome.

Adrenochrome↗
PubMedDate not supplied

[Effect of nonachlazine on ino- and chronotropic function].

As a result of the stimulation of beta-adrenostructures of the myocardium nonachlazin intensifies ino- and chronotropic functions of the heart. This effect does not manifest after administration of practolol and is less pronounced in animals anesthesized with urethane and alpha-chloralose since the sensitivity of the beta-adrenostructures of the myocardium decreases under the influence of the anesthetics. Apart from the stimulation of ino- and chronotropic function of the heart nonachlazin reduces concurrently the intensity of positive chronotropic effect of isoproterenol. Such a combination of the efects called a "partial" beta-adrenoblockade seems likely to play an important role in the manifestation of the antianginal action of nonachlazin.

Anesthesia↗
PubMed1993

Alterations in lipid peroxidation of thrombin-stimulated rat platelets treated with beta-adrenoceptor blocking drugs.

Thrombin-stimulated formation of malondialdehyde in isolated rat platelets was time- and dose-dependent and occurred in parallel with thromboxane B2 production and platelet aggregation. beta-Adrenoceptor blocking drugs inhibited thrombin-stimulated malondialdehyde formation according to their liposolubility in the rank order of potency: atenolol < practolol < oxprenolol < metipranolol approximately alprenolol approximately propranolol. In platelets pretreated with beta-blockers and stimulated with thrombin, a positive correlation was found between malondialdehyde formation and inhibition of aggregation, arachidonic acid liberation from membrane phospholipids as well as thromboxane production. Measurement of malondialdehyde was shown to be an indicator for the arachidonic acid pathway in stimulated and inhibited isolated platelets.

Adrenergic beta-Antagonists↗
PubMed1976

Identification of alpha-adrenergic receptors in uterine smooth muscle membranes by [3H]dihydroergocryptine binding.

[3H]Dihydroergocryptine, a potent alpha-adrenergic antagonist, was used to label smooth muscle membrane binding sites which have the characteristics expected of alpha-adrenergic receptors. Binding of [3H]dihydroergocryptine to rabbit uterine membranes was rapid and reversible with rate constants of 1.26 X 10(7) M-1 min-1 and 0.034 min-1 for the forward and reverse reactions, respectively. [3H]Dihydroergocryptine binding was of high affinity, with an equilibrium dissociation constant (KD) of 8 to 10 nM. Binding was saturable with 0.14 to 0.17 pmol of [3H]dihydroergocryptine bound/mg of protein at maximal occupancy of the sites. No cooperative interactions among the sites were detected. The specificity of the binding sites for a large number of adrenergic agonists and antagonists was identical with the specificity of alpha-adrenergic responses to these agents. The alpha-adrenergic agonist (-)-epinephrine competed for binding with a KD of 0.23 muM. The order of potencies for several adrenergic agonists in competing for the binding sites was (-)-epinephrine greater than (-)-norepinephrine greater than (-)-phenylephrine greater than (-)-isoproterenol in agreement with their alpha-adrenergic potencies. A series of 19 phenylethylamine adrenergic agonists competed for binding in a manner paralleling their potencies as alpha-adrenergic agonists. alpha-Adrenergic antagonists such as phentolamine (KD = 15 nM) and phenoxybenzamine (KD = 18 nM) potently competed for the binding sites. In contrast, beta-adrenergic antagonists such as propranolol (KD = 27,000 nM) and practolol (KD greater than 10(6) nM) did not have high affinity for the binding sites. A series of ergot alkaloids competed for [3H]dihydroergocryptine binding in a manner which paralleled their potencies as alpha-adrenergic agents. Competition for binding sites by alpha-adrenergic agonists and antagonists was a stereospecific process. The (-)-stereoi somers of epinephrine, norepinephrine, and ergotamine were at least 20- to 50-fold more potent than the corresponding (+)-stereoisomers. Compounds devoid of significant alpha-adrenergic activity, such as pyrocatechol, 3,4-dihydroxymandelic acid, normetanephrine, and D-lysergic acid, did not effectively compete for [3H]dihydroergocryptine binding sites. These rabbit uterine binding sites for [3H]dihydroergocryptine appear to have characteristics indistinguishable from those of the physiologically active alpha-adrenergic receptors.

Animals↗
PubMedDate not supplied

Stereospecific binding of timolol, a beta-adrenergic blocking agent.

The beta-adrenergic blocking agent, timolol, appears to be bound to stereospecific as well as nonspecific sites in the particulate fraction (8500g pellet) of the heart, lungs, and brain, whereas the d-isomer of timolol was bound to nonspecific sites only. Timolol disappeared from the particulate fraction at a slower rate than did its optical isomer. At 1 hr after a 0.1-mg/kg dose, the concentration of the l-form in the lung was 1.8 times that of the d-isomer and at 3 and 4 hr the difference was at least 33-fold. The concentration of 14C-timolol in the particulate fraction of rat tissues was inhibited by iv administered timolol and by the l-isomer of propanolol, but not by their corresponding d-forms. Competition for binding sites was dose dependent. Pretreatment with timolol at 0.1 and 5.0 mg/kg reduced the binding of 14C-timolol (dose, 0.1 mg/kg) to lung tissue by 41% and 86%, respectively. In the heart and lung tissue of rats, racemic timolol, propranolol, bunolol, and bunitrolol were approximately equally effective in competing for the binding sites of 14C-timolol. Practolol and sotalol and the beta 2-selective agent butoxamine did not significantly inhibit the binding of 14C-timolol. Similar competition was also observed in the whole brain of rats. This report suggests that the stereospecific binding of timolol may be related to the beta-adrenoreceptor process.

Adrenergic beta-Antagonists↗
PubMed1977

Some effects of pentazocine and cyclazocine on the isolated guinea-pig atria.

Experiments carried out on spontaneously beating and electrically driven guinea-pig atria, have shown that pentazocine and cyclazocine when used in equal concentrations induce a reduction in rate and contraction amplitude. An initial positive inotropic response always precedes with a negative deflection in electrically driven atria. Atropine and nalorphine do not antagonize the drug-induced reduction in rate and contractility. Practolol does not influence either the initial positive or the negative inotropic effects of pentazocine. An apparent tachyphylaxis to the pentazocine-induced positive inotropic response is observed even after the first exposure when the same concentration of pentazocine is tested on the same preparation. Increasing the Ca++ concentration in the medium antagonizes the negative inotropic and chronotropic effects of adenosine and acetylcholine. It is concluded that the negative inotropic effects of the tested drugs may be due to an interference with the Ca++ balance within the atrial cells and/or a direct nonspecific effect on the cell membrane.

Acetylcholine↗
PubMed1977

[Anesthesia in pacemaker implantation. Experiences in 935 cases of anesthesia for the implantation or revision of a cardiac pacemaker].

Observations during 935 anesthesias for implantation or revision of permanent pacemakers are presented. Using different methods of anesthesia we found the light halothane anesthesia introduced by inhalation to be best, provided that only atropine was used for premedication. Applying this method we saw asystolies or ventricular fibrillation in 3% of all cases--3 patients (i.e. 0.4%) died in tabula. Tachycardia (2.4%) occuring mostly during the introduction period were successfully treated by verapamil or practolol. Hypotension (5.4%) mostly took place in the course of anesthesia after implantation of the pacemaker. This depression may be due to a normalisation of the enhanced stroke volume whedication with pethidine or induction with propanidid was followed by comparatively more complications such as exitus letalis (2% resp. 1.5%), cardiac arrest (6.5% resp. 9%) and hypotension (24% resp. 10.5%). Regional anesthesia did not bring specific advantages. The good experiences with soft halothane anesthesia for implantations or revisions of pacemakers include 125 high risk patients (ASA classification IV to VII).

Anesthesia, General↗
PubMed1995

Conformational structure of some beta 1-blockers, their partitioning in lipid and the role of parasubstituents.

The conformational structure of beta1-blockers metoprolol, atenolol and practolol has been investigated by PCILO method. The aminoalkanol moiety adopts the same conformation in all these compounds. These beta-antagonists differ only in the conformation adopted by the substituent para to the aminoalkanol moiety. The graphical representation of the B1-antagonists for the final conformation reveals that only in the S-form, three interacting sites, namely, aromatic moiety, the beta-hydroxyl group and the -NH2(+) groups of aminoalkanol moiety are available for interactions with the receptor. The interaction of the aryloxy oxygen of the beta-antagonists with water molecule has also been taken into account. A linear relationship was obtained between log K (the partitioning of the beta-blocker in DMPC and also in octanol/water) and the potencies of these beta1-antagonists. Possibly, the role of para substituent is to act as an anchor by partitioning in the lipid bilayer so that the beta1-antagonist adopts the proper orientation for binding to the receptor.

Adrenergic beta-2 Receptor Antagonists↗
PubMed1976

Sympathomimetic-induced effects in the soleus muscle of the guinea-pig.

Sympathomimetic amines reduced the peak tension, time to peak and time to half-relaxation of indirectly elicited twitches of the guinea-pig soleus muscle in vivo. Clonic contractions of the soleus muscle were depressed by the amines. On a molar basis salbutamol and orciprenaline were 5.12 and 80.0 times less potent than (+/-)-isoprenaline in producing these effects. Results obtained with the beta-receptor antagonists propranolol, practolol and H35/25 suggest that the depression in skeletal muscle contractility is due to beta2-adrenoreceptor stimulation. The effects of the amines on twitches and clonic contractions of the guinea-pig soleus muscle are qualitatively similar to those reported previously in the cat soleus muscle preparation, which has been used to assess the possible tremorogenic actions of sympathomimetic bronchodilators. On a quantitative basis the molar dose-ratios of the sympathomimetics used, and the effects of beta-receptor antagonists on the responses, are similar in the two species.

Adrenergic beta-Agonists↗
PubMed1977

Effects of adrenalectomy and adrenergic antagonists on potassium metabolism.

We had previously reported that drugs which stimulate beta-2 adrenergic receptors decreased the hyperkalemia produced by infused KCI and thus protected animals against KCI intoxication; these effects were mediated by an action of beta-2 agonists which enhanced tissue uptake of K+. In this study, cats were given an i.v. infusion of KCI which was not lethal in control animals. Acute adrenalectomy markedly increased the hyperkalemic and mortality responses to infused KCI. This impairment in K+ metabolism was corrected by the administration of epinephrine but not by hydrocortisone. Pretreatment with propranolol (which blocks beta-1 and beta-2 receptors) and H35/25 (which blocks beta-2 receptors) produced a similar impairment in K+ metabolism; on the other hand, practolol (which blocks beta-1 receptors) had little or no effect on the mortality and hyperkalemic responses to infused KCI. Evidence that KCI stimulates an adrenal release of catecholamines is presented. This stimulation of adrenal release may be important in conferring resistance to intoxication produced by infused KCI since the released amines can attenuate the KCI-induced hyperkalemia via a beta-2 action which enhances tissue uptake of K+.

Adrenalectomy↗
PubMedDate not supplied

[Mechanism of the antianginal action of nonachlazine].

Experimental data on the mechanism accounting for the action of a new antianginal drug nonachlazine are presented. Nonachlazine was found to intensively (120+/-9.5 per cent) and protractedly (30--40 min) augment the blood flow in the coronary vessels, increasing the oxygen reserve of the myocardium. The contractile function of the heart and beat ejection considerably gain in their intensity, after an initial short-lived fall (by an average of 26.5+/-3.4 per cent), with the resistance of the coronary vessels declining (21+/-1.0 per cent). Administration of nonachlazine made against the background of a propranol (0.5 mg/kg) block of the beta-adrenergic structures of that by practolol (5 mg/kg) is not accompanied by the above effects. The prevalent influence of nonachlazine on the blood circulation and the function of the heart muscle may be explained by its action on the extravascular factors of the venous blood flow regulation (changes in the metabolism activity of the heart, caused by the stimulation of the beta-adrenergic structures of the myocardium).

Angina Pectoris↗
PubMed1976

[Catecholamine metabolism. Physiopathology and pathobiochemistry].

UNLABELLED: Metabolic studies on isolated rat organs showed that vanillyl mandelic acid (VMA) is dehydrogenated by liver homogenate and suspension of pseudomonas fluorescens. In the 100000 g supernatant fraction of homogenated rat kidneys enzymatic activity was sufficient for kinetic studies and the examination of substrate specificity, pH dependence and changes with age and sex of rats. Norepinephrine secretion and resorption may be influenced by antiarrhythmic drugs in vivo: after lidocaine, there was no change of the tyramine dependend norepinephrine depletion of rat hearts, Verapamil inhibited the uptake of norepinephrine by rat hearts. Immobilisation of the animals led to a significant decrease in the myocardial levels for norepinephrine and epinephrine, which was antagonised by recreation of 24 hours. Adumbran prevented the catecholamine depletion, so that the influence of the limbic system may be important for the mediation of sympathetic stimuli. CLINICAL STUDIES: Emotional stress was shown to lead to an elevated plasma level of norepinephrine, cortisole and free fatty acids. In patients undergoing surgery, the application of Valium and Fortral inhibited these stress reactions. After physical stress, which did not lead to significant changes of the catecholamine level in plasma of healthy volunteers, there was an elevated norepinephrine plasma level in patients with cardiac failure, which could be prevented by different antiarrhythmic drugs. The excretion of norepinephrine and VMA of these patients was also increased. It was shown, that sinus rate rose according to norepinephrine levels in plasma in this group, which was contrary to the behaviour of healthy volunteers, showing neither a norepinephrine overflow nor increased heart rate. In patients with atrial fibrillation, AV-conduction also increased with elevated norepinephrine levels in plasma. There was, however, no direct correlation. Determination of the cardiac AV-difference of plasma-norepinephrine levels showed a cardiac catecholamine overflow, which could be inhibited by specific and nonspecific antiarrhythmic drugs (Verapamil, Practolol). In studies of catecholamine and glucocorticoid metabolism, no significant difference of catecholamine and VMA could be determined in patients with normal blood pressure and arterial hypertension. There was, however, a tendency to increased values in patients of the last group. In postural hypotension, plasma levels and urinary excretion of catecholamines were decreased and showed no variation after physical stress in orthostasis and after nicotine. In patients with tumors of the adrenal cortex and medulla, a close relation of the disturbance in catecholamine and corticoid metabolism was revealed.

Animals↗
PubMed1976

The protective effects of methysergide, 6-hydroxydopamine and other agents on the toxicity of amphetamine, phentermine, MDA, PMA, and STP in mice.

The ability of various drugs to prevent the lethal effects of 4-methoxyamphetamine (PMA) and 3, 4-methylenedioxyamphetamine (MDA) were reduced by pretreatment with phentolamine and 6-hydroxydopamine suggesting that release of norepinephrine from peripheral adrenergic nerves contributed to their toxicity. Pretreatment with methysergide reduced the lethal effects of (+)- and (-)-amphetamine, MDA, PMA and 2, 5-dimethoxy-4-methylamphetamine (STP) suggesting that an action on serotonergic receptors contributed to their toxicity. Pretreatment with 4-chloroamphetamine, practolol and haloperidol did not alter the lethal effects of the agents studied.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMedDate not supplied

Differential effects of propranolol on lymphocyte rosette formation and response to plant mitogens.

The effects of propranolol on various lymphocyte functions were studied to gain a better understanding of the recently demonstrated suppressive effect of propranolol on rheumatoid factor production. D- and L-propranolol at a concentration of 1 X 10(-4)M inhibited the formation of human EA rosettes. The inhibition occurred within one minute of adding the compounds, was reversible, and did not affect cell viability. Addtion of propranolol to preformed EA rosettes failed to disaggregate them. Patching and capping of SIg by an Fab'2 anti-IgG were inhibited at 2.5 X 10(-5)M and above. Propranolol at 2.5 X 10(-5)M also inhibited lymphocyte response to phytohemagglutinin and pokeweed mitogen without evidence of cell toxicity by trypan blue staining or absolute numbers of surviving cells. Congeners of propranolol with mainly beta adrenergic blocking properties did not show inhibitory effects. The inhibitory activities of propranolol are interpreted in terms of propranolol's membrane stablizing effects and ability to interfere with membrane receptor movement.

Animals↗
PubMedDate not supplied

The pharmacokinetics of oral and intravenous prenalterol in young, healthy volunteers.

The pharmacokinetics of prenalterol in healthy young volunteers after i.v. and oral dosing has been studied. There is evidence of non-linearity following the i.v. dosing. Evidence of dose-dependent pharmacokinetics following i.v. dosing has been obtained. The sustained-release formulation is very effective: almost 12 h were needed to achieve 50 per cent of the total AUC.

Administration, Oral↗