Biomedical subjects
Publications and source records attributed to A G Burm.
The gas chromatographic determination of volatile organic anaesthetic agents in blood and in respiratory gases is described. The analysis in blood is based on a head space technique. Sampling of inspired and end-tidal gases is carried out by means of a system including a gas sampling valve.
In 14 mongrel dogs wash-in and wash-out curves for halothane were obtained from measurements of arterial blood, mixed venous blood and end-tidal gas. From a certain point in the wash-in period the halothane concentration of arterial blood can be calculated from the halothane concentration in end-tidal gas and the blood-gas partition coefficient for halothane. Analysis of the curves shows that they are composed of two exponential components suggesting the presence of two body compartments. The question of a two-compartment system versus a multi-compartment system in discussed.
A literature survey indicates that some complaints occur relatively frequently among anesthetists and nurses working in operating rooms. Pollution of the air in the operating rooms by anesthetic gases is often considered as a possible cause. On account of this the degree of pollution has been determined. Concentrations of nitrous oxide and halothane were measured using an infrared absorption spectrophotometer. In each room the concentrations were measured at several different sites. In naturally ventilated operating rooms the concentrations increased steadily during operation. The measured values lied mostly between 1500 and 3000 ppm (vol/vol) for nitrous oxide and between 15 and 35 ppm for halothane. In mechanically ventilated operating rooms where no recirculation is applied a constant level was found some time after the beginning of an operation. The concentrations varied from about 100 to 500 ppm for nitrous oxide and from 1 to 5 ppm for halothane. In naturally ventilated operating rooms the anesthetic gases were rather homogeneously spread, while in mechanically ventilated rooms there was an inhomogeneous distribution. Scavenging of waste anesthetics is recommended.
The pharmacokinetics of lidocaine and bupivacaine and tri-deuteromethyl-labelled lidocaine and bupivacaine were investigated in healthy volunteers. The deuterium-labelled and the unlabelled form of the drug to be investigated were simultaneously infused in 10 min. Plasma concentrations were determined using a combination of capillary gas chromatography and mass fragmentography. Bi-exponential functions were fitted to the plasma concentration-time data. The mean distribution and elimination half-lives were 8.4 +/- 5.9 min and 96 +/- 26 min for lidocaine, 9.2 +/- 7.0 min and 98 +/- 27 min for deuterium-labelled lidocaine, 15.3 +/- 9.9 min and 111 +/- 32 min for bupivacaine, and 15.2 +/- 10.9 min and 109 +/- 31 min for deuterium-labelled bupivacaine, respectively. The mean volumes of the central compartment and mean steady state volumes of distribution were: lidocaine 37 +/- 151 and 97 +/- 201, deuterium-labelled lidocaine 39 +/- 161 and 98 +/- 181, bupivacaine 27 +/- 111 and 66 +/- 231 and deuterium-labelled bupivacaine 28 +/- 121, and 65 +/- 221, respectively. The respective mean plasma clearances were 0.88 +/- 0.181 min-1, 0.87 +/- 0.181 min-1, 0.61 +/- 0.151 min-1, and 0.62 +/- 0.171 min-1. The results of the study indicate that substitution of a deuterated methyl group does not alter the pharmacokinetics of lidocaine and bupivacaine in healthy subjects.
Effects of aging on the onset of early signs of central nervous system (CNS) toxicity, associated total and free arterial threshold serum concentration, and the disposition of bupivacaine were studied in eight younger (11-15 years) and eight older (16-28 years) rhesus monkeys. Bupivacaine was infused at a rate of 0.15 mg/kg minute until unceasing movements of the eye, oscillating from side to side and up and down (nonpositional nystagmus). This was regarded as an objective sign of early CNS toxicity. Most animals showed drowsiness and sedation by the end of the infusion. CNS toxicity occurred significantly faster (p less than 0.025) in the younger (13.7 +/- 2.5 minutes) than in the older (17.1 +/- 2.6 minutes) animal group. A significant correlation was found between the onset time of CNS toxicity and age. The coefficient of determination (R2) for this correlation was 0.48. Also, the dose associated with the onset of CNS toxicity was significantly smaller in the younger (2.06 +/- 0.38 mg/kg) than in the older (2.60 +/- 0.39 mg/kg) animals. However, the total and free arterial threshold serum concentration of bupivacaine was similar in both groups. Age did not influence the disposition of bupivacaine.