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PubMed1975

Idiopathic paroxysmal ventricular tachycardia in infants and children.

Seven children with idiopathic PVT ranging in age from one day to 18 yr, have been observed during the past three years. The presenting complaints and frequency of paroxysms varied greatly. Three patients presented with syncope; four were asymptomatic. Lidocaine was effective in terminating acute symptomatic attacks; procaine amide and propranolol were effective in long-term control of the arrhythmia. Monitoring of the dynamic ECG was invaluable in establishing the diagnosis, characterizing the arrhythmia, and evaluating the effects of activity and therapy.

Adolescent↗
PubMed1978

Pulmonary absorption of drugs in the neonatal rat.

To compare the pulmonary absorption of drugs in newborn rats (3-27 days old) with that in adults, 0.01-0.1 ml of Krebs-Ringer phosphate solution (pH 7.4) containing a drug was administered to anesthetized animals by way of a catheter introduced through a tight-fitting tracheal cannula. After various times, lungs and trachea were removed and assayed for drug that remained. Semilogarithmic plots of percent drug remaining against time yielded a straight line for each compound. The lipid-soluble drugs procaine amide and sulfisoxazole were absorbed at similar rates in newborn and adult rats. In contrast, the lipid-insoluble drugs tetraethylammonium, p-aminohippuric acid, and mannitol were absorbed approximately 2 times more rapidly in younger rats (3-12 days) than in older animals (18 day, 27 day, or adult). The results suggested that the respiratory tract membranes of 3- to 12-day-old rats have a greater porosity than those of older animals.

Absorption↗
PubMed1978

Effect of thyroxine on permeability of the neonatal rat lung to drugs.

The effect of thyroxine (1-2 microgram/g i.p. on days 1-4 after birth) on development of adult-type permeability characteristics in the lung was investigated in rats 6-18 days of age. In both treated and control rats, the lipid-soluble drug procaine amide was absorbed at similar rates in all age groups. In contrast, in thyroxine-treated animals, pulmonary absorption rates for the lipid-insoluble compounds mannitol and p-aminohippuric acid declined to adult levels at age 6-12 days, 6 days earlier than in controls. Thyroxine treatment thus accelerates development of adult permeability characteristics in the pulmonary epithelium.

Aminohippuric Acids↗
PubMed1970

Effect of lidocaine on the electrophysiological properties of ventricular muscle and purkinje fibers.

Preparations of right ventricular papillary muscle and false tendon (Purkinje fiber) were obtained from dog hearts, placed in a bath perfused with Tyrode solution, and observed both under control conditions and during exposure to lidocaine in concentrations from 1 x 10(-7) to 5 x 10(-4) mole/liter. Transmembrane voltages were recorded from both ventricular muscle (VM) and Purkinje fibers (PF) of spontaneously beating and electrically driven preparations. Low concentrations (1 x 10(-6) and 1 x 10(-5) mole/liter) attenuated or abolished phase 4 (diastolic) depolarization and spontaneous firing in PF without decreasing their diastolic excitability. Concentrations of 1 x 10(-5) mole/liter produced maximal shortening of both action potential duration (APD) and effective refractory period (ERP) and made the ERP long relative to APD; the latter alteration was more prominent in VM. At concentrations </= 1 x 10(-5) mole/liter, lidocaine either caused a slight increase or no change in peak maximum rate of phase 0 depolarization (V(max)) and membrane responsiveness, the relationship between transmembrane activation voltage (MAV) and V(max) of the resultant action potential; these concentrations had no significant effect on resting potential (RP) in VM, maximal diastolic transmembrane voltage (DTMV(max)) in PF, or action potential amplitude in either fiber type. High (toxic) concentrations (>/= 1 x 10(-4) mole/liter) did not cause further shortening of APD or ERP in either VM or PF but did produce a decrease in peak V(max) of phase 0 and membrane responsiveness. In most cases, these concentrations also caused a decrease in RP or DTMV(max) and action potential amplitude, with progression to bizarre action potential depolarization and inexcitability. These properties of lidocaine are strikingly different from those of quinidine or procaine amide. The mechanisms responsible for lidocaine's in vivo antiarrhythmic action are discussed.

Action Potentials↗
PubMed1976

Mechanism of supraventricular tachycardia and pharmacological effects on it.

Electrophysiologic study in 30 patients with documented SVT, 16 of whom had preexcitation, and in 24 control subjects were reported. The mechanism of SVT were found to be various and to include reentry confined to the AV node, SA node or the atrium, reentry through accessory pathway and ectopic atrial automaticity. It was noted that some of SVT might use concealed accessory pathway in VA direction while the some of SVT in WPW syndrome might not utilize accessory pathways. Electrophysiological properties in cases with SVT did not differ from those observed in controls. There were no differences in the mode of electrophysiological action of drugs between XVT and control groups. Both propranolol and procaine amide slightly depressed AV conduction. However, the action of the drugs on echo zone were not the same. The basic mechanisms of the action of the drugs in SVT were discussed.

Heart Conduction System↗
PubMed1977

Arrhythmias in the post CCU phase of myocardial infarction: their correlation with the acute illness.

To estimate the frequency of potentially life-threatening arrhythmias in myocardial infarction following transfer from the coronary care unit (CCU) and to identify features of the acute illness which predict such events, 66 patients were monitored on-line by means of a computer assisted system. Premature ventricular contractions (PVCs) were detected following transfer from the CCU in 64 patients (97%). In 29 (44%) they fell in classes 2 to 4 of Lown. Accelerated ventricular rhythm was detected in five and ventricular tachycardia in three. The presence of these rhythm disturbances did not correlate with age, sex, infarct location, the occurrence of previous infarction, the level of serum cardiac enzymes, the presence of heart failure, atrial arrhythmias, heart block, or serious ventricular arrhythmia in the CCU. Use of procaine amide or quinidine for persistent ventricular arrhythmia in the CCU was correlated with detection of class 2, 3 or 4 PVCs. Thus, PVCs are nearly universal in the late phase of hospitalization for myocardial infarction. Frequent and complicated PVCs are common and occur most frequently in individuals in whom such events have been persistent in the CCU.

Acute Disease↗
PubMed1984

Effects of butylated hydroxytoluene (BHT) on biliary excretion of xenobiotics and bile flow in rats.

A significant enhancement in the biliary excretion of iv injected sulfobromophthalein (BSP), phenol- 3,6 -dibromphthalein disulfonate (DBSP), procaine amide ethobromide (PAEB) and ouabain was observed in rats maintained on diets containing 0.25% BHT for periods of 10 days. The enhanced biliary excretion of these drugs in BHT treated rats appears to be correlated with the increase in bile flow produced by BHT. The increased bile flow was due to an increase in canalicular bile production rather than a change in net ductular secretion or reabsorption of fluid since bile to plasma concentration ratios of erythritol were unchanged and no permeability change in the biliary tree was observed when mannitol was administered by retrograde intrabiliary injection. The increase in bile flow was not due to an enhanced excretion of bile salts into bile, because both the biliary bile acid concentration and total biliary excretion of bile acids were lower in BHT-treated rats than in control rats. It appears that the increase in bile flow produced by BHT is due to the osmotic choleresis related to the secretion of BHT and its metabolites into bile.

Animals↗
PubMed1975

Survival of an oral surgery patient with malignant hyperthermia.

Malignant hyperthermia is a life-threatening complication of general anesthesia. Its cause is not precisely known but it appears to be related to a genetic defect that allows increased release or decreased reaccumulation of calcium by the sarcoplasmic reticulum whech then results in a hypermetabolic state. As with any unexpected complication when a patient is under general anesthesia, early diagnosis and treatment are essential. The early clinical signs that the surgeon and anesthesiologist shoulc be alert to are unexplained tachycardia, unexplained tachypnea, muscular rigidity, and increased temperature. Therapy should be accurate and immediate. The essentials of therapy are discontinuance of the anesthetic agent; immediate, active, and aggressive cooling; administration of procaine or procaine amide, 1 mg/kg/min until the pulse slows; correction of electrolyte and acid-base imbalances; maintenance of urinary output with furosemide and large volumes of fluids, intravenously; and supportive care. A thorough knowledge of the management of malignant hyperthermia ahd the pathophysiology of the complications that may occur with general anesthesia will allow the oral surgeon to fully meet his obligations to his patients.

Acid-Base Equilibrium↗
PubMed1976

Adverse reactions to drugs: relationship to immunopathic disease.

Immunopathic disease resulting from drug treatment occurs when drugs interact with lymphoid cells and induce an immunological reaction. Drugs, being foreign to the body, are immunogenic, either as such or as haptens bound to carrier proteins. The immune response is usually innocuous or unnoticed but occasionally becomes pathogenic. The impact is especially obvious when the immunopathic response affects blood, skin, liver or kidney. Immunopathic responses and effector mechanisms of injury, whether to drugs or other antigens, are considered in terms of four types: Type I--anaphylactic and mediated by immunoglobulin (Ig) E antibody, and exemplified by immediate penicillin reactions; Type II--cytolytic and complement-associated, mediated by IgG antibody, and exemplified by haemolytic reactions; Type III--vasculonecrotic (Arthus reaction), mediated by immune complexes, and exemplified by serum sickness-like reaction; Type IV--delayed hypersensitivity involving T lymphocytes but no antibody, and exemplified by contact dermatitis. In addition, certain drugs induce true autoimmune reactions exemplified by reactions to procaine amide (lupus erythematosus) and alpha methyldopa (positive Coombs test result). Drug reactions must be interpreted in terms of modern immunology, with involvement of both the B and T lymphocyte systems. Inherited predisposition exists, probably dependent both on immune response genes and on the rate of enzymatic handling of drugs. Diagnosis depends on a carefully taken history of drug administration, recognition of clinical manifestations, and results of tests now available in departments of clinical immunology.

Aged↗
PubMed1989

[Intracellular recording of myotonia in mdx mouse and the effect of Ca antagonist in myotonia].

Bulfield and others found X-linked muscular dystrophic (mdx) mouse by screening C57 BL/10 mice. The serum CK and PK are high in mdx mice, and they develop muscle degeneration 10-15 days after birth. The regeneration is vigorous in mdx mice and almost all the muscle fibers are replaced by regenerated fibers by 60 days after birth. Although mdx mice have been developed as a model for X-linked muscular dystrophy we have found that myotonic bursts are recorded when a glass microelectrode is inserted into the muscle fibers of hemidiaphragm preparations of mdx mice. Insertion myotonia is ceased by addition of the Na channel blocker tetrotoxin. Myotonia is not reduced, nor ceased by lowering the extracellular Ca to 1/15 of the volume of ordinary Tyrode's solution. Calcium antagonist, nicardipine at the dose of 10(-7), and 10(-6)M/L do not reduce myotonic bursts. Higher dose of nicardipine up to 2 x 10(-5)M/L abolished myotonic bursts. These results indicate that myotonic bursts are related to muscle membrane abnormalities, and each action potential occurs through Na channel, but not through Ca channel Higher dose of calcium antagonist can abolish myotonia by affecting Na channel in addition to their primary effects of Ca channel. The clinical effects of the Ca antagonist for myotonia was reported in one study. Since previous medications for myotonia including quinine HCl, procaine amide, diphenylhydantoin, and carbamazepine have some side effects such as tinnitus, headache, nausea, cardiac blocks, and bone marrow suppression, Ca antagonist may be used as a safe therapeutic drug for myotonia.

Animals↗
PubMed1984

Cardiac and antiarrhythmic effects of imipramine in patients with ventricular arrhythmias.

Imipramine is an effective antiarrhythmic agent against ventricular arrhythmias and complex features of ventricular premature depolarizations at plasma concentrations ranging from 100 to 400 ng per ml. Imipramine's effects on the electrocardiogram are similar to procaine amide and quinidine producing a slight prolongation of PR and QRS intervals. A relatively long half-life of elimination, mean = 9 + 3.7 hours, and no significant adverse effect on left ventricular function suggest imipramine will be useful even for patients with depressed cardiac function.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

The search for new antiarrhythmics in the group of chirally 1,2-aminoalcohols. I. 3',4',5'-trimethoxybenzoic acid esters of optically active N,N'-dimethyl-N,N'-bis-(1-hydroxybutyl-2) ethylenediamines.

Both enantiomeric (2S, 2'S) and (2'R) N, N'-dimethyl-N, N-bis (1-hydroxybutyl-2)-ethylenediamines (Table 1) were obtained by methylation of the corresponding N,N'-ethylene-bis-2-aminobutanols-1. The esterification of the former aminoalcohols with 3, 4, 5-trimethoxybenzoic acid gave the both enantiomeric in title named esters (Table 2). The isomer with S configuration at both chirally center (C2 and C2), has a particularly strong antiarrhythmic properties (about 10-20 greater than quinidine or procaine amide in different experimental arrhythmia models in animals. The 2R,2'R enantiomere is 10-100 times less active one. It seems that the antiarrhythmic activity of this new group of antiarrhythmically active compounds, derivatives of chirally 1, 2-aminoalcohols is connected with spatial configuration.

Amino Alcohols↗
PubMedDate not supplied

Pharmacological properties of Craviten (M-71).

The preparation Craviten (M-71) produced by POLFA Pharmaceutical Works in Cracow (2S, 2'S) N, N'-dimethyl-N, N'-bis-[1-(3',4',5'-trimethoxybenzoyloxy)-butyl]-2-ethylenediamine dihydrochloride) prevents and abolishes heart rhythm disturbance induced in the rat with BaCl2, CaCl2, adrenaline or aconitine. The doses effectively preventing arrhythmia development were in the range from 0.035 to 0.175 mg/kg. They are many times lower than the doses of lidocaine, hexobendine, procaine amide and D,L-propranolol producing a similar effect. Craviten has a much more favourable therapeutic index than these antiarrhythmic agents. Craviten causes sinus bradycardia and slows down myocardial conduction. It exerts a spasmolytic effect about 70 times as strong as papaverine. It has no influence on the central nervous system, on urine excretion, and after topical application it has no irritating or local anaesthetic effect. The 2R, 2'R isomer of Craviten has a similar profile of pharmacological action but its antiarrhythmic and spasmolytic effects are many times weaker.

Animals↗
PubMedDate not supplied

The effect of a new antiarrhythmic drug: Craviten (M-71) on the ATP level in heart muscle slices in vitro.

Under anaerobic conditions, in which glucose is the only energy source, the ATP level in heart muscle slices diminishes to about 50% of the control value during 60 min of incubation. The presence of a new antiarrhythmic drug, Craviten (Polfa) (2S, 2'S) N, N'-dimethyl-N, N'-bis-[1(3', 4', 5'-trimethoxybenzoyloxy)-butyl-2]-ethylenediamine dihydrochloride, (M-71), and to some extent also its 2R, 2'R isomer in 10 times greater concentration protects against this spontaneous ATP fall observed anaerobically in the control experiments. Under aerobic conditions, with glucose or palmitate as energy sources, Craviten even raises the ATP level in comparison to the initial control values. This effect is stereospecific, since the 2R, 2'R isomer does not change the aerobic ATP level, Quinidine and procaine amide used for comparison as standard antiarrhythmic drugs do not counteract the anaerobic ATP decrease, and under aerobic conditions they even enhance the ATP fall. Craviten, a new antiarrhythmic drug, exerts some stereospecific effect on energy metabolism and the ATP content in heart muscle slices in vitro.

Adenosine Triphosphate↗
PubMed1977

Hepatic uptake of foreign compounds: influence of acute extrahepatic biliary obstruction.

Extrahepatic cholestasis produced by bile duct ligation decreased the net hepatic uptake of organic anions including sllfobromophthalein, sulfobromophthalein glutathione and phenol-3,6-dibromophthalein disulfonate, and the neutral organic compound, ouabain. The net hepatic uptake of procaine amide ethobromide, an organic cation was not similarly affected. Impairment of net hepatic uptake by bile duct ligation was demonstrated by reduced liver concentration and content of administered compound despite higher plasma concentration. Acute bile duct ligation did not alter the amount of hepatic cytoplasmic anion binding proteins. The impaired net hepatic uptake of sulfobromophthalein in bile duct-ligated rats was reversed by re-establishing bile flow. Deleterious effects of endogenous bile or bile constituents and specific alteration of membrane carrier proteins are considered possible contributing factors to the impaired net hepatic uptake process observed in bile duct-ligated rats.

Animals↗