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PubMed1977

[Drug-induced disorders of lupus erythematosus type (author's transl)].

Drug induced Lupus erythematosus (LE)-like syndromes are generally observed after long-term and/or high-dose therapy with so called "principal inducers" procainamide, hydralazine, isoniazide, chlorpromazine, anticonvulsives and possibly with D-penicillamine, too, and even so in some cases after some additional 26 drugs. The rare pseudo LE syndrome appears after combined drugs which usually contain pyrazolone derivatives used especially against venous diseases. The mechanism of induction of autoimmune reactions in these disorders varies and is after all still unknown. There are individual differences in drug metabolism, genetic disposition for increased autoantibody formation and sometimes humoral and cellular immune reactions against the drug itself. Essentially involved in the indication of autoimmune reactions is often the production of hapten carrier complexes between drugs and body constituents and drug induced changes of autoantigen elimination as well as drug mediated immunologic imbalance.

Animals↗

PubMed1980

Stability of standard curves prepared for EMIT homogeneous enzyme immunoassay kits stored at room temperature after reconstitution.

We examined the stability of standard curves obtained with use of homogeneous enzyme immunoassay reagents (EMIT; Syva Corp., Palo Alto, CA) for assay of lidocaine, procainamide, N-acetylprocainamide, gentamicin, and theophylline, when stored at room temperature (23-24 degrees C) after reconstitution of the lyophilized materials. Standards were run and curves obtained for as long as 16 days after reconstitution. All standard curves were acceptable, according to the criteria specified in Syva product literature. Absorbance changes for all calibrators, including the zero calibrator, increased gradually with time. Increases of non-zero calibrators were largely offset by a parallel increase in the zero calibrator, such that the quantity delta A--delta A0 was very nearly constant with time. Standard curves based on the quantity delta A--delta A0 can be used for longer than curves based only on delta A.

Acecainide↗

PubMed1983

[Autonomic effects of scaritoxin in the cat and guinea pig. Cardiac protection by an anti-arrhythmia agent].

A purified extract from the muscles of the fish Scarus gibbus (93% scaritoxin and 7% ciguatoxin) was tried on anesthetized cats and isolated guinea-pig atria. Intra-venous injection to cats (10, 20 and 40 mg/kg) induced deep respiratory depression, inhibition of duodenal contractions, increased salivary secretion, mydriasis and lacrymal secretion. Heart rate was slowed by 17 to 44 per cent. Impaired cardiac conduction led to different types of blocks. On the contrary, cardiac excitability was enhanced, as evidenced by the occurence of many auricular and mostly ventricular extra-systoles, often evolving into long periods of ventricular paroxysmal tachycardia. The rate of contraction of isolated guinea-pig atria was equally depressed and this effect was antagonized by atropine. The duration of the refractory period was shortened; an inotropic effect was observed and the action of acetylcholine was potentiated by the toxin. Cholinesterase inhibition by scaritoxin, previously mentioned in other papers, is thus evidenced. Mydriasis and duodenal inhibition may be tentatively explained by a nicotinic effect on the sympatheticoadrenal system. This mechanism may be responsible for cardiac inotropic action and increased excitability. Other mechanisms may be suggested, including a possible digitalis-like effect due to a cyclopentanone ring in the scaritoxin molecule. Interestingly, intra-venous injections of the antiarrythmic drug procainamide (20 to 30 mg/kg) could either prevent or reverse the signs of cardiac hyperexcitability in the anesthetized cat. However, death results usually from respiratory depression, the intimate mechanism of which is not yet known.

Animals↗

PubMedDate not supplied

[Lymphocytic and lymphocytoactive components in the etiopathogenic mechanisms of systemic lupus erythematosus. An analysis of the literature].

Lymphocyte populations play an important role in the mechanism of autoantibody induction, mainly of antinuclear ones, in such collagen diseases as S.L.E. Aetiology and pathogenesis of SLE are multifactorial: genetic predisposition, lupogenic factors (among them the hormonal ones) with direct and indirect action on B and T lymphocytes, conditioning the production of lymphocytotoxins and antibodies against blood cells. Subjects carrying the HLA DRW3 antigen have three to four times more probabilities to get a S.L.E. In the serum of SLE patients as well as in their relatives auto-or heterolymphocytotoxic antibodies are present, directed against the antigens of the HLA complex. There is evidence that antilymphocyte antibodies appear in patients with procainamide induced SLE, as well as anti-IgG - and antierythrocyte antibodies; this fact is due to the impairment of the immunologic regulation. Concerning the circulating immunocomplexes (CIC) in idiopathic S.L.E., it was observed that they increase in patients with active SLE, but there is no statistical evidence of a significant inverse proportional rate of these parameters. The role of CIC in SLE induction is bound with T lymphocyte subsets.

Animals↗

PubMed1984

Tubular transport and metabolism of cimetidine in chicken kidneys.

Renal tubular transport and renal metabolism of [14C]cimetidine (CIM) were investigated by unilateral infusion into the renal portal circulation in chickens (Sperber technique). [14C]CIM was actively transported at a rate 88% that of simultaneously infused p-aminohippuric acid, and its transport was saturable. The following organic cations competitively inhibited the tubular transport of [14C]CIM with decreasing potency: CIM, ranitidine, thiamine, procainamide, guanidine and choline. CIM inhibited the transport of [14C]thiamine, [14C]amiloride and [14C]tetraethylammonium. During CIM infusion, two renal metabolites, CIM sulfoxide and hydroxymethylcimetidine, were found in urine. When CIM sulfoxide was infused, its transport efficiency was 32% and not saturable. CIM sulfoxide did ot inhibit the simultaneous renal tubular transport of p-aminohippuric acid or tetraethylammonium. CIM is transported by the organic cation transport system and the kidney metabolizes CIM. Transport of CIM and other cationic drugs could produce a drug interaction to alter drug excretion.

Animals↗

PubMed1984

[Drug-induced lupus erythematosus syndrome. Pathogenesis and relation to systemic lupus erythematosus].

The drug-induced lupus erythematodes syndrome is a heterogeneous group of exogenically caused transitory autoimmunopathies . Essential knowledge has been got concerning the pathomechanism of the syndromes evoked by hydralazine, procainamide, diphenylhydantoin and Venopyronum . Though there are analogies to the systemic lupus erythematosus, we must take into consideration a diversity of diseases. Antibodies against histone have a certain diagnostic as well as pathogenetic relevance.

Diagnosis, Differential↗

PubMed1984

Treatment of cardiac arrhythmias in dogs with gastric distention-volvulus.

Lidocaine, procainamide, quinidine, or a combination of these drugs was used to treat a variety of cardiac arrhythmias in 70 dogs with gastric distention-volvulus. Antiarrhythmic drugs were administered by constant infusion, the double-infusion technique, or intramuscular injection. Most cardiac arrhythmias were ventricular in origin, although supraventricular arrhythmias including atrial fibrillation also were included. Normal sinus rhythm was reestablished in greater than 85% of the dogs treated. Restoration to normal rhythm was improved by combination drug therapy, normalization of acid-base balance, and appropriate electrolyte therapy.

Animals↗

PubMed1981

[Determination of plasma concentrations of anti-arrhythmia agents].

The measurements of the plasma concentrations of antiarrhythmic drugs is useful both for studying the pharmacokinetics and bio-availability of a drug, and for assessing the relationship between pharmacological activity and plasma levels in clinical practice so that dosages may be adapted to obtain optimal efficacity in each individual patient and to avoid side-effects caused by drugs with low therapeutic indices. Many methods are available, including spectrophotometry, spectrofluorometry, gas chromatography, liquid chromatography and immuno-enzymology. The practicability, sensitivity and specificity of these techniques are compared with respect to their objectives. Particular attention is paid to the principal antiarrhythmic agents with fairly well defined zones of efficacity: procainamide, quinidine, disopyramide, propranolol, lignocaine and mexiletine.

Anti-Arrhythmia Agents↗

PubMed1978

[Malignant hyperthermia in a black child. A case report].

A case of malignant hyperthermia in a Black boy is presented. He developed this condition during repair of a cleft palate, with halothane as the triggering agent. The importance of the high incidence of malignant hyperthermia in patients with certain musculoskeletal abnormalities is stressed. Despite a cool and well air-conditioned theatre, the patient's temperature was 41 degree C when the condition was suspected. At that stage general muscle rigidity was present. The patient was successfully treated with procainamide, sodium bicarbonate and hydrocortisone; surface cooling (with ice packs) was instituted and the stomach was washed out with ice-cold Ringer's solution. Over a period of 14 days serum creatine phosphokinase values decreased from 630 IU (on the day of the incident) to 12 IU. A muscle biopsy showed variation in muscle fibre size. Electron microscopical studies showed myofibrillar disruption and folding of the basement membrane. A modified version of Denborough's technique was used for the in vitro exposure of muscle strips to halothane and suxamethonium. Isometric contraction was measured and recorded. A severe contraction followed the exposure of muscle strips to halothane, which confirmed the diagnosis.

Child↗

PubMed1980

Drug effects on autoantibodies and immune complexes.

In connective tissue diseases, putatively immunosuppressive drugs may lower antinuclear antibody (ANA), anti-DNA antibody and rheumatoid factor titres. Penicillamine may induce or increase titres of antinuclear and/or anti-muscle antibodies. The mechanism of induction of penicillamine antinuclear autoimmunity evidently differs from that seen with hydrallazine and procainamide. While the latter may induce circulating immune complex formation, the effect of penicillamine on circulating immune complex levels in rheumatoid arthritis is variable. Our recent findings will be discussed.

Acetylation↗

PubMed1980

Drug-induced pancreatitis: a critical review.

We critically reviewed the English language literature pertaining to drug-induced pancreatitis and attempted to determine whether the reported association between each drug and pancreatitis was valid. The following drugs seem to cause pancreatitis: azathioprine, thiazides, sulfonamides, furosemide, estrogens, and tetracycline. Less convincing, but suggestive evidence exists for: 1-asparaginase, iatrogenic hypercalcemia, chlorthalidine, corticosteroids, ethacrynic acid, phenformin, and procainamide. Evidence implicating other drugs is either inadequate or contradictory. Little is known about the pathogenesis of drug-induced pancreatitis. Ethanol was not considered in this review.

Acetaminophen↗

PubMed1981

Experience with immunological tests in drug-induced hepatitis.

Nine patients are reported who developed hepatic injury following the administration of therapeutic agents. The drugs incriminated were prajmalium bitartrate (4 patients), quinidine (3 patients), procainamide and nifedipine (one patient each). In all patients the clinical features indicated an allergic process, which in three cases was substantiated by positive response to reexposure. The detection of immunologic processes in our patients by various in vitro methods supports the assumption that immune mechanisms may be involved in the production of drug-induced hepatic disease and confirm allergy.

Aged↗

PubMed1982

Effect of antiarrhythmic drugs on In-111-labeled leukocytes: chemotaxis and adherence to nylon wool.

The influence of lidocaine (L) and procainamide (P) on the chemotactic ability and adherence to nylon wool of In-111-labeled human polymorphonuclear leukocytes (PMNs) was investigated. At the normal therapeutic levels of L (0.022 mM whole blood) or P (0.03 mM whole blood) no change in PMN function was observed. However, at and above five times the aforementioned blood levels of L, significant reduction in the chemotactic ability of PMNs was noted (p less than 0.005). The adverse effects of In-111 radiation appeared insignificant at all L or P concentrations during the 3-hr observation period. The labeled PMNs were resistant to the toxic effects of a higher concentration of P than that of L, and the reduction in PMN chemotaxis and adherence to nylon wool was not apparent until the P concentration reached 1.5 mM.

Cell Adhesion↗

PubMed1982

Effect of arterial-venous plasma concentration differences on the determination of mean residence time of drugs in the body.

Using dogs or rabbits as model animals the effect of arterial-venous plasma concentration differences of propranolol, procainamide, griseofulvin, furosemide and theophylline on the determination of mean residence time (MRT) following intravenous administration was evaluated using standard methods. The MRT values calculated from femoral venous data were always higher (ranging from 1.5 to 109%) than those from femoral arterial data. The differences were mainly attributed to the additional residence time of drugs in the sampling tissue (leg). From a physiological point of view it appears generally more logical to assume that only the MRT calculated from arterial data using conventional methods represents the "true" MRT in the body. The potential pharmacokinetic significance of the present findings is discussed. New approaches, which eliminates the effect of arterial-venous plasma concentration differences on the MRT determination, are proposed.

Animals↗

PubMed1981

Arterial-venous plasma concentration differences of six drugs in the dog and rabbit after intravenous administration.

The arterial blood from the femoral artery and venous blood from the femoral vein wee simultaneously collected following intravenous administration of propranolol, lidocaine, procainamide, furosemide, theophylline and griseofulvin to dogs or rabbits. The preliminary results of arterial-venous (A-V) plasma concentration profiles are reported in this communication. The maximum A/V ratios shortly after a rapid intravenous bolus dose were 277-, 15-, 34-, 33-, 5.4- and 3240-fold, respectively, for the above six drugs. The venous plasma levels were higher than arterial plasma levels during parallel terminal phase by as much as 104, 48, 134, 29, 16, and 47%, respectively, for the above six drugs. These data suggest a very rapid and extensive uptake of the drugs by the sampling tissues (the leg) shortly after dosing. The potential significance of A-V differences in pharmacokinetic and pharmacodynamic studies are briefly discussed.

Animals↗

PubMed1995

Mechanism of drug-induced lupus. I. Cloned Th2 cells modified with DNA methylation inhibitors in vitro cause autoimmunity in vivo.

Treating activated CD4+ T cells with DNA methyltransferase inhibitors modifies gene expression and induces autoreactivity. Adoptive transfer of viable polyclonal autoreactive cells causes a lupus-like disease, most likely because of one or more effector functions expressed by the autoreactive cells. However, the number of potential effector mechanisms expressed by polyclonal cells is large. To more readily identify responsible mechanisms, we asked if autoimmunity can be induced by using the conalbumin-reactive, cloned Th2 cell line D10.G4.1, treated with 5-azacytidine (5-azaC) or procainamide (Pca). Treated, but not untreated, cells responded to syngeneic APCs without Ag, overexpressed LFA-1, spontaneously lysed syngeneic macrophages, and secreted relatively large amounts of IL-6, small amounts of IL-4, and no detectable IL-2 nor IFN-gamma. Adoptive transfer of treated, but not untreated, cells induced a severe immune complex glomerulonephritis, pulmonary alveolitis, central nervous system abnormalities including fibrinoid necrosis, karyorrhexis, and meningitis, and bile duct proliferation with periportal inflammatory cell infiltration resembling primary biliary cirrhosis. Anti-ssDNA, anti-dsDNA, and anti-histone Abs were also found. These experiments demonstrate that modification of this cloned T cell line with DNA methyltransferase inhibitors is sufficient to cause an autoimmune disease, with features of lupus as well as autoimmune liver disease. The results also raise the possibility that macrophage lysis, IL-6 secretion, and LFA-1 overexpression could contribute to the disease process. This system may be useful in testing the role of these and other pathologic mechanisms in the development of specific autoimmune lesions.

Animals↗

PubMed1995

Morphological changes in human erythrocytes induced in vitro by antiarrhythmic drugs.

Several hypotheses suggest that the molecular mechanism of action of class I antiarrhythmic drugs (AAD) involve non-specific interactions of these compounds with phospholipid bilayers of the myocardial membrane that surround and functionally modulate ion transport by sodium channels. As a result of these interactions the channel function would be altered. To probe the validity of these hypotheses three AAD with different degrees of lipophilicity were made to interact in vitro with human erythrocytes in a wide range of concentrations. The most lipophilic drug was asocainol (ASOC), the least one was procainamide (PROC) while the lipophilicity of the third, quinidine (QUIN), lay somewhere between the other two. The observations made by scanning electron microscopy (SEM) showed that the three AAD produced profound shape alterations to the incubated erythrocytes. However, the type and intensity of these changes were dependent on the drug under study and its concentration.

Anti-Arrhythmia Agents↗

PubMed1993

[Effects of 6,7-dimethoxycoumarin on experimental arrhythmia].

By using the arrhythmic animal models, the effect of 6,7-dimethoxycoumarin (DMOC) on arrhythmia was investigated. The arrhythmia in anaesthetized rat were induced by iv aconitine 20 micrograms.kg-1 or CaCl2 5 mg.kg-1. The arrhythmia in anesthetized guinea pigs was induced by iv ouabain 3.6 micrograms.kg-1.min-1. Procainamide (PA) was used as a positive control. DMOC (33-500 mg.kg-1, ig) and PA (100-800 mg.kg-1, ig) in anaesthetized rats could delay the time of onset of arrhythmia induced by aconitine. The ED50 of DMOC and PA for postponing the occurrence of ventricular extrasystole (VE) were 88 mg.kg-1 (95% confidence interval was 43-165 mg.kg-1) and 183 mg.kg-1 (95% confidence interval was 109-304 mg.kg-1), respectively. The results suggested that the anti-arrhythmia potency of DMOC was higher than that of PA (P < 0.01).

Aconitine↗