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PubMed1979

Identification of the polypeptide chains in Torpedo californica electroplax membranes that interact with a local anesthetic analog.

Procaine amide azide, a derivative of the local anesthetic procaine amide, was prepared and its interactions with acetylcholine receptor-rich membrane fragments from Torpedo californica electroplax were studied. Procaine amide azide was radiolabeled by a method that may be of general use for the preparation of other radioactive tertiary amines. When low concentrations of 3H-labeled procaine amide azide were photolyzed in the presence of receptor-rich membrane preparations, a simple pattern of incorporated radioactivity was seen after electrophoresis on sodium dodecyl sulfate/polyacrylamide gels. Only two major labeled bands were seen, corresponding to apparent Mr of about 43,000 and 90,000. When the length of the gels was increased, the labeled band of lower Mr was resolved into two labeled proteins, one major and one minor, with apparent Mr of 43,000 and 40,000, respectively. The radioactivity incorporated into the protein of Mr 40,000 could be attributed to interaction of [3H]procaine amide azide with cholinergic ligand-binding sites, whereas labeling of the polypeptide of Mr 43,000 appears to represent interaction of the photolabile derivative with another class of sites. The labeling component of 90,000 Mr could be removed by preparation of membrane fragments in iodoacetamide-containing buffer and therefore appeared unrelated to the acetylcholine receptor.

Affinity Labels↗
PubMed1976

Effect of oxygen toxicity and nitric acid-induced lung damage on drug absorption from the rat lung.

To investigate the effect of pulmonary oxygen toxicity and nitric acid-induced lung damage on absorption of drugs from the lung, rats were either exposed continuously to approximately 100% oxygen or given an intratracheal injection of 1% nitric acid solution (0.15 ml), and rates of drug absorption from damaged and control lungs were compared after various times. To measure pulmonary absorption rates, 0.1 ml of drug solution (0.1-10 mM) was administered through a tight-fitting tracheal cannula to anesthetized animals, and, after various times, lungs were assayed for unabsorbed drug. Drugs investigated were procaine amide ethobromide, p-aminohippuric acid, procaine amide and mannitol-14C. Rates of drug absorption were increased 1.1-1.2 fold after 48-54 hrs of continuous oxygen exposure and 1.3-1.6 fold at 1-4 days after nitric acid treatment. The results suggest that both types of lung damage increase the porosity of the absorbing membrane, and that nitric acid damage also alters the integrity of lipoid regions of the membrane.

Absorption↗
PubMed1976

Effect of paraquat-induced lung damage on permeability of rat lung to drugs.

To investigate the effect of paraquat-induced lung damage on pulmonary absorption of drugs, rats were given a single oral dose of paraquat (250 mg/kg), and rates of drug absorption from damaged and control lungs were compared after various times. To measure absorption rates of drugs, 0.1 ml of 10 mM drug solution was administered through a tracheal cannula to anesthetized animals and, after various times, lungs were assayed for unabsorbed compound. Drugs investigated were procaine amide ethobromide, p-aminohippuric acid, and procaine amide. Rates of drug absorption increased 1.4-2.8-fold at 3.5 days after paraquat administration and returned to near control values by the 15th day. The results suggest that paraquat-induced lung damage increases the porosity of the pulmonary epithelium.

Aminohippuric Acids↗
PubMedDate not supplied

Influence of quinidine on ATP-linked calcium binding by heart mitochondria and microsomes.

The action of quinidine on heart microsomal and mitochondrial calcium binding in the presence of MgATP was studied under different experimental conditions and compared with other antiarrhythmic agents such as procaine amide and lidocaine. Quinidine stimulated microsomal calcium binding but depressed mitochondrial calcium binding. Although procaine amide stimulated microsomal calcium binding, it did not affect mitochondrial calcium binding. On the other hand, lidocaine depressed calcium binding by mitochondria without affecting calcium binding by the microsomal fraction. The stimulation of microsomal calcium binding by quinidine was not apparent at high concentrations of Mg2+, low concentrations of ATP, or low concentrations of Ca2+. The depressant action of quinidine on mitochondrial calcium binding was not observed at low concentrations of Mg2+ or ATP but was more pronounced at low concentrations of Ca2+. These results suggest that the action of quinidine on mitochondria may play a major role in eliciting cardiodepressant effect.

Adenosine Triphosphate↗
PubMed1975

Wolff-Parkinson-White syndrome: mechanocardiographic study on the mechanical consequences of ventricular pre-excitation.

To elucidate the mechanical consequences of ventricular pre-excitation in patients with the W,W syndrome, electrical and mechanical events in the ventricles during anomalous pathway conduction and normal atrioventricular conduction were examined mechanocardiographically in 11 cases of Group A and 19 cases of Group B, in whom anomalous pathway conduction was stopped by procaine amide, resulting in normalization of conduction. Eight healthy persons were employed as a control group. In the control group, procaine amide had no significant effect on the mechanocardiographic values. In the WPW syndrome, significant prolongation of the P-X, P-J, P-T, P-C, P-I, P-Ao, and P-II intervals was induced by the drug. From the results of statistical analyses of measured values, it would appear that mechanical events in the ventricles were accelerated by ventricular pre-excitation but the extent of acceleration of the former was less than the extent of prematurity of the latter. The anomalous ventricular pre-excitation occurred earlier in cases of Group B than in those of Group A, while initiation of ventricular contraction, atrioventricular valve closure, and aortic vlave opening were accelerated more in Group A. In one case of Group B, electrical phenomena could not be related to mechanical events.

Adult↗
PubMed1976

Enhanced pulmonary absorption of drugs in rats with experimental silicosis.

To investigate the effect of pulmonary silicosis on absorption of drugs from the lung, rats were given an intratracheal injection of 50 mg quartz dust, and rates of drug absorption from silicotic and control lungs were compared at 60 and 120 days after treatment. The pulmonary absorption of procaine amide ethobromide and p-aminohippuric acid was increased by 33-41% in animals with silicosis, whereas absorption of procaine amide in silicotic animals was not significantly different from control. The results suggest that silicosis results in an increased porosity of the pulmonary epithelium.

Aminohippuric Acids↗
PubMed1961

A comparison of tests for antifibrillatory action.

THE OBJECT OF THE EXPERIMENTS WAS TWOFOLD: first, to choose the most satisfactory test for antifibrillatory action; secondly, to place several drugs with reputed antifibrillatory activity in an order of potency as a preliminary to investigating their mode of action. Measurements were made on isolated rabbit atria at 34 degrees C of (1) the maximum driving frequency the atria would follow, (2) conduction velocity, (3) contractions, and of the threshold for the production of (4) extrasystoles, (5) flutter and (6) fibrillation. Log dose-response curves were plotted for quinidine, papaverine, procaine, dibenamine and procaine amide. The maximum frequency test and fibrillation threshold test gave similar results with all the drugs, and the results gave the order quinidine 1.0, procaine 0.53, Dibenamine 0.47, papaverine 0.43 and procainamide 0.26. Thresholds for extrasystoles and flutter were much more variable. The regressions relating changes in conduction velocity and contraction to log dose were different from those for maximum driving frequency and fibrillation threshold for procaine, papaverine and dibenamine, but the regressions for quinidine and procaine amide were nearly parallel in all tests. Serpajmaline contained a substance with antifibrillatory activity as great as that of quinidine and with no greater depressant action on contractions.

Animals↗
PubMed1975

Effect of papain-induced emphysema on permeability of rat lung to drugs.

To investigate the effect of a papain-induced emphysema-like condition on pulmonary absorption of drugs, rats were exposed to either papain aerosol or distilled water aerosol (control) intermittently for 2 wk, and rates of drug absorption from damaged and control lungs were compared. To measure absorption rates, 0.1 ml of drug solution (0.1-10 mM) was administered through a tracheal cannula to anesthetized animals, and after various times lungs were assayed for unabsorbed compound. In absorption experiments with the lipoid-insoluble compounds, mannitol, p-aminohippuric acid, and procaine amide ethobromide, all three drugs were absorbed from the lungs about twice as rapidly in papain-treated rats as in control. In contrast, procaine amide, a relatively lipoid-soluble drug, was absorbed at the same rate in both control and papain-treated animals. The results suggest that papain-induced lung damage increases the porosity of the pulmonary epithelium.

Aerosols↗
PubMed1975

Arrhythmia prophylaxis: Long-term suppressive medication.

The author describes the notions that led to initiation of controlled trials of long-term medication with antiarrhythmic drugs following myocardial infarction, and reviews reports of controlled trials with diphenylhydantoin, alprenolol, and procaine amide. It is concluded that, so far as possible widespread prophylactic use of these drugs to prevent sudden death is concerned, diphenylhydantoin has no place, while procaine amide cannot be evaluated on a large scale because of the frequency with which it causes serious adverse reactions. There is no bar to an extended trial with alprenolol or comparable beta-blocking drugs. The author believes that nonspecific prophylactic long-term use of antiarrhythmic drugs to prevent sudden coronary death outside the hospital is unlikely to prove rewarding.

Acute Disease↗