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At least 73 records · Page 4Linked to original sources
PubMed1991

[Transient liver damage due to prajmalium bitartrate].

3 patients developed transient cholestatic jaundice after administration of prajmalium bitartrate, a class I antiarrhythmic drug. The leukocyte inhibition tests showed 4%, 12% and 15% inhibition, respectively, while eosinophilia was seen in all 3, supporting the assumption that the transient hepatic damage was due to drug exposure. Discontinuing the drug resulted in improvement in the clinical and biochemical findings.

Adult↗
PubMed1990

[Opposite control of O2 affinity for hemoglobin by donors and acceptors].

The effects of electron donors and acceptors on O2 binding by hemoglobin were studied. 2,4-Dinitrophenol, levomycetin and pelargonidine-3,5-diglycoside which act as electron acceptors in free radical reactions, enhance this process. In contrast, N-propylajmalin which is known to be an electron donor in the above reactions, suppresses the O2 binding. Diphosphoglycerate and inositol hexaphosphate, the natural inhibitors of O2 binding, exhibit, similar to N-propylajamlin, the properties of electron donors, the latter being a more potent electron donor than the former.

2,4-Dinitrophenol↗
PubMed1990

[Effects of N-propylajmaline bromide and trimecaine combination on normal and abnormal automatism of Purkinje fibers in dogs and arrhythmias at the late stage of experimental myocardial infarct].

Prajmalium bromide in combination with trimecaine was tested for effects on arrhythmias in the late period of canine experimental myocardial infarction. The combination given in subthreshold doses was found to restore sinus rhythm in 8 of 11 cases. It also decreased the maximum repolarization rate in rat papillary muscles to a greater extent than either drug given alone. The rate of spontaneous firing of Purkinje fibers from the ischemic zone was decreased by the combination of the drugs.

Animals↗
PubMed1990

[Effect of N-propylajmaline bromide on the normal and abnormal automatism of Purkinje fibers in the dog].

The effects of prajmalium bromide on normal and abnormal automaticity were studied in Purkinje fibers from dog hearts at late stages of experimental myocardial infarction. Prajmalium bromide (1.2 micromol/l) moderately reduced the frequency of normal and abnormal automaticity by 16 and 20% respectively. Prajmalium bromide induced early after-depolarizations, increased the frequency of spontaneous firing and decreased the maximum diastolic potential in the fibers that initially developed the automaticity of an intermediate type between normal and abnormal. It is suggested that antiarrhythmic effects of prajmalium bromide in the late stage of experimental myocardial infarction are not related to the influence of the drug on the abnormal automaticity in Purkinje fibers.

Action Potentials↗
PubMed1985

[Differences in the action of Ca2+ ions on a cumulative Na-channel blockade due to tertiary and quaternary amines].

In voltage-clamp experiments on frog myelinated fibres it has been established that the increase in Ca2+ concentration from 2 to 20 mM does not effect the use-dependent (cumulative) inhibition of sodium channels (INa) produced by the tertiary local anesthetics (lidocaine, tetracaine, etidocaine) and the quaternary antiarrhythmic drug N-propyl ajmaline (NPA). The NPA-induced inhibition of sodium channels does not undergo any essential changes as the (Ca)0 is raised from 2 to 20 mM. On the contrary, the cumulative blockade produced by the tertiary local anesthetics under such an elevation of the (Ca)0 is sharply reduced. This reduction is caused by the inhibitory action of the (Ca)0 on the local anesthetics-induced transition of sodium channels from the state of rapid to slow inactivation. The (Ca)0 does not affect the interaction of the quaternary NPA with open sodium channels. The data obtained provide evidence in favour of the hypothesis about the existence of the different binding sites responsible for cumulative blockade of the INa induced by tertiary and quaternary amines.

Amines↗
PubMed1985

[Localization of the binding site for quaternary derivatives of ajmaline in the Na channel of an excitable membrane].

The effects of external or internal application of quaternary derivatives of ajmaline and N-propyl ajmaline (NMA) to the frog nodes of Ranvier were studied by the voltage clamp method. It was established that external application of NMA is much less effective than that of the tertiary amine ajmaline or its quaternary analog N-ethyl ajmaline at comparable concentration. Even at a concentration of 1 mM NMA when applied externally caused only relatively insignificant tonic and use-dependent inhibition of sodium currents. In contrast, internal application of NMA (1 mM) through the cut ends of the fiber led to pronounced use-dependent inhibition of sodium currents. The conclusion is drawn that the binding site for NMA is located in the inner mouth of the Na channels which becomes available for the charged blocker only after opening of the activation gate.

Ajmaline↗
PubMed1986

[Comparative study of the anti-arrhythmia effect of flecainide acetate and prajmalium bitartrate in patients with tachycardiac ventricular rhythm disorders].

In an open randomized therapeutic study, 20 patients known to have frequent ventricular premature beats (VPB) and/or ventricular pairs (VP) were treated with both 2 X 200 mg flecainide (F) and 4 X 20 mg prajmalium-bitartrate (P) for 3 months each. There was a drug-free interval of one week between the two therapy phases. 24-hour long-term ECG-registrations were carried out before the start of the therapy phases as well as 1 week, 1 month, 2 months and 3 months after the initiation of antiarrhythmic therapy. After one week, the group as a whole evidenced a VPB reduction of 94% under F and only 57% under P (p less than or equal to 0.05). The percentage of individual patients in whom there was a statistically significant VPB reduction was also higher under F than under P (65% vs. 40%). In the group as a whole, there was a VP reduction of 99% under F and 88% under P (p less than or equal to 0.05) after one week. Of the 13 individuals with frequent VP (over 16 VP/24 h), a significant reduction was seen in 77% under F and only 38% under P. The difference between the two antiarrhythmic agents registered after one week was also observed in the further course of therapy but could no longer be statistically confirmed for the ventricular pairs. An aggravation of ventricular arrhythmias was observed in 2 patients under F and in 3 under P.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Dose-effect relation of N-prajmalium bitartrate with control of plasma levels].

15 patients with ventricular ectopic beats classified to at least Lown class III with more than 100 ventricular ectopic beats in one hour were treated with N-prajmalium bitartrate (NPAB) in increasing dosages. The first dosage of 4 X 5 mg/d has been increased by 5 mg in three steps of three days to a level of 4 X 20 mg/d. A resting ECG, the systolic time intervals and a 24 h ECG were registered before treatment and after every dose. The median PQ time increased from 170 msec to 200 msec, the increase becoming significant (p less than 0.05) with a dose of 4 X 5 mg/d NPAB and above. Frequency, QRS and the frequency-corrected QT time did not change significantly. At a dose of 4 X 10 mg/d NPAB the increase of the quotient pre-ejection period to ejection time PEP/LVET became significant, increasing continuously from 0.35 to 0.48. Six of the 15 patients showed a significant reduction of ventricular ectopic beats, couplets and salvoes. In two patients the antiarrhythmic effect was significant at 4 X 5 mg/d. With an increasing dose from 4 X 10 mg/d each responder showed a significant reduction of ventricular ectopy. The lowest effective plasma concentrations ranged from 15 to 213 ng/ml with a median value of 58 ng/ml and an upper quartile of 94 ng/ml. There was no significant difference in plasma concentrations between responders and non-responders.

Aged↗
PubMed1989

[Modification of blood coagulation by the anti-arrhythmia drug prajmalium bitartrate in vivo].

We studied the effects of prajmaliumbitartrate (PBT, Neo-Gilurytmal, Giulini Pharma, Hannover, FRG), an antiarrhythmic drug on some parameters of blood coagulation in patients. PBT, 20 mg given three times a day, significantly prolonged template bleeding time and ex vivo thrombus formation time in a modified Chandler's loop. Ex vivo platelet aggregation using different agonists and tests of the plasmatic coagulation system remained unchanged.

Ajmaline↗
PubMed1989

[The effect of the antiarrhythmic, prajmalium bitartrate, on human thrombocyte function].

Studies of the in vitro effects of the antiarrhythmic drug prajmalium bitartrate (PBT, Neo-Gilurytmal) showed inhibitory effects on platelet aggregation and thromboxane production. PBT inhibited the primary and secondary phases of aggregation induced by adrenaline (epinephrine) or adenosine diphosphate (ADP). Platelet aggregation stimulated with collagen, platelet activating factor (PAF), and the thromboxane mimetic 9,11-azo-prostaglandin H2 (U 44064) was inhibited. The secondary phase of aggregation induced by ristocetin and aggregation caused by arachidonic acid (AA) were inhibited in samples from some donors (responders) but not in others (nonresponders). Platelet aggregation by the ionophore calcimycine (A 23187) was not inhibited, but small doses of calcimycine abolished the PBT-induced inhibition of aggregation caused by ADP. Thromboxane production of platelets with collagen of ADP was inhibited by higher concentrations of PBT, whereas AA-induced thromboxane synthesis remained unchanged. The observed antiplatelet activities of PBT are thought to result from calcium and sodium channel blocking properties of the drug.

Ajmaline↗
PubMed1986

[The effect of Neo-Gilurytmal on heart lesions induced with isoprenaline].

Influence of Neo-Gilurytmal was studied upon catecholamine heart lesion in rats of two weight categories: In bigger ones (350-420 g) the lesion was diminished, in smaller animals (200-230 g) any protective influence did not occur. Sensitivity of myocardium to Neo-Gilurytmal is supposed to concur with that to catecholamine effect in rats of increasing weight.

Ajmaline↗