[Repeated driving under influence]. / Gjentatt kjøring i påvirket tilstand.

Many drivers arrested for driving under the influence have earlier been arrested and convicted for a similar type of violation. The article reviews Norwegian studies on car drivers influenced by alcohol, other drugs than alcohol, and also drivers influenced by amphetamine. The results show that between 10 and 30% of drivers convicted for driving under the influence of alcohol, are rearrested two or more times for the same violation during a subsequent three year period. The recurrence rate is dependent on blood alcohol concentration at the selection time. The recurrence rate among drivers under the influence of drugs other than alcohol is significantly larger (up to 54%), when studied over the same three year period. The number of drivers influenced by amphetamine has increased dramatically during recent years. The recurrence rate among drivers influenced by amphetamine is on part with that of drivers using other drugs than alcohol. There are indications that an increasing number of drunken drivers have changed their abuse pattern during recent years from alcohol to illegal drugs such as amphetamine.

Study of rearrests for drunken driving in Norway.

The National Institute of Forensic Toxicology (NIFT) in Oslo receives blood samples from all Norwegian drivers suspected of driving under the influence of alcohol. It is well known that a large proportion of the arrested drunken drivers are repeat offenders. The purposes of this investigation was to find the arrest rates (the percentage of subjects arrested once or more) among drunken drivers followed retrospectively and prospectively during the 11-year period 1984-1994 and the probability of 'abstaining' from becoming a recidivist during the 9 years subsequent to the year of selection. By examining the rearrest rates during the 3 following years for drivers selected in 1986, 1989, 1991 and 1992 we tried to look for major effects due to the change in the Norwegian road traffic act of 1988. Altogether 45% of the selected drunken drivers were arrested two or more times. Totally the '9-year survival rate' (i.e. not being rearrested) was 60% for drivers with blood alcohol concentration (BAC) selected from the interval 0.06-0.09%; 56% from BAC 0.13-0.16% and 51% from 0.26-0.29%. The data were further evaluated with respect to frequency of rearrest during 3 years after selection, and was around 30% in 1986, while it was lower for drivers selected in 1992 (19%). An explanation for the reduction in rearrest rate may be the changes in the road traffic act which took place in 1988.

Recidivism among drunken and drugged drivers in Norway.

The prevalence of re-arrest among drunken drivers in relation to different blood alcohol concentrations (BAC) at the time of the offences was studied. Between 38 and 50% of arrested drunk drivers were re-arrested for similar offences. The frequency of re-arrests was, however, reduced during 1992 compared with a986, but only significantly for those with a low BAC interval (60-90 mg/d). We conclude that drivers with high re-arrest rates have a careless attitude to the Road Traffic Act and require a different treatment and follow-up programme.

Incidence of alcohol and drugs in fatally injured car drivers in Norway.

Blood samples from 159 fatally injured drivers from 1989 and 1990, corresponding to 57% of all fatally injured drivers in Norway during this period, were analysed for alcohol and psychoactive drugs. Alcohol was found in 28.3% of the drivers, 27.0% above the legal limit of 0.05%. Drugs were found in 16.4% of the drivers; benzodiazepines and tetrahydrocannabinol were the drugs most frequently found. Among 79 drivers fatally injured in single-vehicle accidents, 41.8% were positive for alcohol and 21.5% were positive for drugs.

Amnesic effects and subjective ratings during repeated dosing of flunitrazepam to healthy volunteers.

Flunitrazepam (1 mg) or placebo was administered once daily over a treatment period of 8 days to healthy, male volunteers to study the time course of the effects on memory functions and on subjective ratings of alertness and tension. The plasma level of flunitrazepam increased by approximately 40% (P < 0.05) during the treatment period. The mean pre-dose level of flunitrazepam on day 4 and day 8 was approximately 0.005 microM, and no residual effects on memory functions were observed. Intake of flunitrazepam decreased the number of freely recalled words by about 85% (P < 0.05) and significantly affected the subjects' rating of attention when tested during the first few hours after drug intake on day 1 of treatment. However, no significant effect on the subjects' rating of relaxation was observed. When tested similarly after 8 days treatment, flunitrazepam significantly affected the subjects' rating of relaxation (P < 0.01). Furthermore, no tolerance developed for the effect of flunitrazepam on free recall (P > 0.3) and the subjects' rating of attention (P > 0.7), and these effects had nearly equal time courses during the treatment period. This may indicate that the amnesic effect of benzodiazepines is at least partially mediated through the effects on attention or general arousal. Two of the subjects in the active drug group reported adverse reactions or incidents of discomfort during the 1st week following the treatment period, whereas none in the placebo group reported such reactions.

An animal model of postmortem amitriptyline redistribution.

An experimental rat model was developed to study postmortem changes of drug concentration after an acute overdose. Overnight fasted rats were fed 75 mg of amitriptyline (AMI). Two h after dosing, the rats were anaesthetized and blood samples were drawn from the femoral vein (peripheral blood--PB) and the heart (HB). The rats were sacrificed by CO2 and left at room temperature for either 0.1, 0.5, 1, 2, 5, 10, 24, 48, or 96 hours, when samples of heart blood, blood from the inferior vena cava (PB) and tissue samples from different liver lobes, heart, lungs, kidney, thigh muscle, and brain were taken. Samples were analyzed by high performance liquid chromatography. The AMI concentration in HB increased fairly rapidly within the first 2 h postmortem and from then the average ratio was 6.4 +/- 0.8 (mean +/- sem) (n = 31). In PB, the post/antemortem AMI concentration ratio followed an approximately exponential rise; at 2 h postmortem the ratio was 1.6 +/- 0.3 (n = 5), and at 96 h 55.1 +/- 23.8 (n = 4). For the main metabolite nortriptyline (NOR), the concentration changes followed the same pattern, but to a lesser extent. Among the tissues, the liver lobes had high, but variable drug concentrations; lobes lying closest to the stomach had the highest drug concentrations. The drug concentration in the lungs declined significantly. This animal model demonstrates postmortem drug concentration changes similar to those described in humans. Probable mechanisms include drug diffusion from the stomach and GI tract to the surrounding tissues and blood; and postmortem drug release from the lungs and possibly other drug-rich tissues into the blood.

Measuring ethanol in blood and breath for legal purposes: variability between laboratories and between breath-test instruments.

We determined the concentrations of ethanol in nearly simultaneous specimens of venous blood (BAC) and end-expired breath (BrAC) after healthy volunteers drank moderate amounts of alcohol. BAC was measured at two laboratories and BrAC was analyzed with two instruments (Intoxilyzer 5000) from the same manufacturer. The mean difference in BAC between laboratories was 0.0105 mg/g (SD 0.0219); 95% of the differences ranged from -0.0333 to 0.0543 mg/g. The mean difference in BrAC between instruments was 0.0153 mg/L (SD 0.0136), and 95% of the differences ranged from -0.0119 to 0.0425 mg/L. The coefficient of variation (CV) between laboratories was 2.9% compared with 4.5% between breath-test instruments. Venous BAC (y) and BrAC (x) were highly correlated (r = 0.978). However, when the Intoxilyzer instruments indicated that BrAC had reached zero, the actual BAC was 0.135 mg/g, according to the average forensic laboratory reports. The Intoxilyzer 5000 breath analyzers used in this study seem to have a constant analytical bias.

Diffusion as a mechanism of postmortem drug redistribution: an experimental study in rats.

In some cases of drug overdose there is a reservoir of unabsorbed drug in the stomach and gut. Furthermore, agonal aspiration might establish a second reservoir in the lungs. Two experimental rat models were used to study if diffusion from these reservoirs could contribute to the phenomenon of postmortem drug redistribution. Overnight fasted rats were sacrificed by CO2 and 75 mg of amitriptyline (AMI) was administered by a gastric tube. In the first series (n = 19), the tubes were removed after AMI administration. In the second series (n = 17), the trachea was ligated and cut prior to drug administration to prevent airways contamination. The rats were left at room temperature on their back for a period of 5, 10, 24, 48, 96 up to 192 h and samples of heart blood, blood from the inferior vena cava, tissue samples from heart, lungs, different liver lobes, kidney and psoas muscle were taken. In both series of rats we observed that as early as 5 h postmortem increasing concentrations of amitriptyline were found in the liver lobes lying closest to the stomach. In rats where the trachea was not ligated, drug contamination of the lungs also resulted in an increase in drug concentration within 5 h in heart blood and heart muscle. In rats where the trachea had been ligated, amitriptyline was found in the lungs after 96 h postmortem. The main metabolite nortriptyline was also detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Oral administration of codeine in the presence of ethanol: a pharmacokinetic study in man.

Three healthy male volunteers were given a codeine (1 mg/kg) solution in the absence and presence of ethanol in a cross-over designed study. The blood ethanol concentration was kept at approximately 16 mM for 8 hrs. Blood samples were taken at several occasions during the first day after the codeine administration. Urine was sampled during three days. There were no significant differences in the area under serum concentration versus time curve in the absence and presence of ethanol with respect to free codeine, total codeine and total morphine. The fraction of codeine glucuronized in serum (approximately 94%), the maximum serum concentration of free (0.34 microM) and total codeine (6.3 microM), the time to reach the maximum serum concentration values (approximately 65 min.) were also similar in the absence and presence of ethanol. The accumulated percentage of the codeine dose given which was found as codeine and morphine and their conjugates in the urine ranged from 50 to 91 percent in the different subjects. The accumulated percentage of the administered codeine dose found as free morphine in the urine, was significantly lower in the ethanol exposed individuals (0.18 +/- 0.03%) compared to the controls (0.39 +/- 0.09%). The percentage of the codeine dose found in the urine in the control situation as free codeine (5.2 +/- 2.2%) was not statistically different from the amount found in the urine after ethanol treatment (4.3 +/- 2.0%). The percentage glucuronized morphine (95.3 +/- 0.4%) and codeine (91.9 +/- 2.2%) in the urine in the absence of ethanol was similar to glucuronized morphine (95.3 +/- 2%) and codeine (93.1 +/- 3%) after ethanol exposure.(ABSTRACT TRUNCATED AT 250 WORDS)