ABSTRACT
Plasma glyceryl trinitrate (GTN) concentration was studied in 12 volunteers producing gun powder. Serial blood samples were obtained from the cubital vein before and during work at two sites of production; high concentrations of GTN were detected in the plasma. Control specimens from a femoral vein contained much less GTN, indicating that blood in the cubital vein was enriched by dermally absorbed GTN. In the roll mill area concentrations of GTN in the cubital vein were higher than in the press area, but individual factors were also important since some workers consistently had higher concentration of GTN than others. Differences in absorption were more important than differences in the metabolism of GTN since only a small variation in disappearance rate was found after a sublingual test dose of GTN. Moderate changes in pulse rate and blood pressure were noted during the day. The major discomfort experienced was a headache that increased during working hours, but this was not significantly related to GTN concentrations in the air or in the blood from the cubital vein. The observations imply that major efforts should be made to reduce dermal contact with GTN during production work.
Subject(s)
Chemical Industry , Headache/chemically induced , Nitroglycerin/blood , Occupational Diseases/chemically induced , Adult , Air/analysis , Blood Pressure/drug effects , Environmental Exposure , Female , Humans , Kinetics , Male , Middle Aged , Nitroglycerin/adverse effects , Nitroglycerin/analysis , Pulse/drug effectsABSTRACT
The atrial effective (ERP) and relative (RRP) refractory periods were examined at high atrial pacing rates in 12 patients before and after intravenous injection of propranolol, and in 5 patients before and after injection of verapamil, using the technique of paired pacing. Seven of the patients had A-V block grade II-III and 10 patients had sinus rhythm. The range of atrial ERP in all patients was found to be 200 to 270 msec. and the range of atrial RRP was 230 to 330 msec. The atrial ERP and RRP were longer at a pacing rate of 160 per minute than at a pacing rate of 240 per minute. The conduction delay between the second impulse and the atrial depolarization was found to be due to increased interval between the stimulus and the start of the depolarization wave. The atrial ERP increased after injection of propranolol in 8 of 12 patients, decreased in 3 patients and was unchanged in one patient. The atrial RRP increased in 7 patients, decreased in one patient and was unchanged in 4 patients. In all patients the changes were of moderate degree. The conduction delay between the stimulating impulse and the atrial response was shorter after propranolol in 7 patients, longer in one patient and unchanged in 4 patients. The ERP of the atrioventricular conducting tissue was 220 to more than 380 millisec. After injection of propranolol it increased in all of 3 patients in whom it could be measured. After injection of verapamil no significant effects on the atrial ERP and RRP were found. ERP of the atrioventricular conducting tissue was lengthened in 4 of 5 patients, and the degree of A-V block during rapid atrial pacing increased after injection of verapamil. It is suggested that the effect of propranolol on atrial arrhythmias is due to its effect on ectopic pacemaker activity rather than any effect on the refractory period of the atrium. The effects of verapamil on the atrioventricular conducting tissue may explain some of the antiarrhythmic effects of this drug.