PubMed · 13110478
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D J CURTIS. The drinking driver.. https://pubmed.ncbi.nlm.nih.gov/13110478/
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Repeated exposure to drugs of abuse results in an increased sensitivity to their behavioral effects, a phenomena referred to as behavioral sensitization. It has been suggested that the same neuroadaptations underlying behavioral sensitization contribute to the maintenance and reinstatement of addiction. Dysregulation of dopamine (DA) neurotransmission in the mesoaccumbens system is one neuroadaptation that is thought to lead to the compulsive drug-seeking that characterizes addiction. Evidence that sensitization to psychostimulants and opiates is associated with an enhancement of drug-evoked DA levels in the nucleus accumbens has also been obtained. Like other drugs of abuse, the acute administration of ethanol (ETOH) stimulates DA release in this brain region. Moreover, repeated ETOH experience results in an enhanced behavioral response to a subsequent ethanol challenge. Data regarding the influence of repeated ethanol intoxication and withdrawal upon mesoaccumbal DA neurotransmission is limited. Studies examining ETOH-evoked alterations in mesoaccumbal DA neurotransmission as a function of withdrawal duration are lacking. The present experiments quantified basal and ethanol-evoked DA levels 14 days and 24 h following the cessation of a repeated ETOH intoxication protocol, which results in sensitization to the locomotor activating effects of ethanol. Locomotor activity was assessed in parallel groups of animals. Studies were conducted in two mouse strains, C57BL/6J and DBA/2J, which differ in their behavioral responses to ETOH. The results indicate the development of transient tolerance to both ETOH-induced behavioral activation and evoked accumbens DA release at early withdrawal. Moreover, no enhanced DA response to a subsequent ETOH challenge could be demonstrated in ETOH experienced animals 2 weeks after withdrawal, in spite of the observation of clear behavioral sensitization at this time point. These results suggest that, at least in the case of ethanol, sensitization of the DA mesolimbic system may not be necessary for the development of behavioral sensitization.
Spinal epidural haematomas (sEDH) can be regarded as rare events, in principle a spontaneous and a traumatic aetiology can be distinguished. Spontaneous spinal epidural haematomas can arise, e.g. from vascular malformations, coagulopathies, etc. On the other hand, traumatic sEDH are related to, e.g. spinal trauma or intraoperative vascular injuries. With regard to clinical significance, spinal epidural haematomas accompanied by transient mild neurological symptoms up to lethal outcomes have been observed. We report on a 53-year-old male alcoholic who was found in the kitchen of his asylum in a grotesquely fixed body position, with his head and cervical spine in a maximum anteflected position. A general practitioner had ruled for a non-natural manner of death due to "broken neck" and alcohol intoxication, therefore, the prosecution authorities called for a medicolegal autopsy. At autopsy, paravertebral soft tissue haemorrhage in between the shoulder blades was disclosed. Furthermore, a spinal epidural haematoma, extending from the foramen magnum down to the middle portion of the thoracic spine was found. No fractures of vertebrae nor lesions of spine ligaments or bleedings of intervertebral discs were found. Blood alcohol concentration was determined 1.92 g/l and urine alcohol concentration was 1.76 g/l. Further morphological findings were cerebral oedema and cardiac hypertrophy; the urinary bladder was found filled to bursting. Neuropathological investigations confirmed the presence of the spinal epidural haematoma and assigned lethal significance to this finding. There were no histological signs of axonal injury. Reconstruction revealed that when sitting on a chair in a drunk condition, the individual's upper part of the body had fallen backwards in the corner and subsequently got stuck with maximum anteflection of the head and cervical spine, causing rupture of vessels and spinal epidural haematoma. Acute respiratory failure caused by impairment of the phrenic nerve following spinal epidural haematoma with potential synergism of alcohol intoxication was ascertained as the cause of death.
OBJECTIVES: Ethanol intoxication has hemodynamic and metabolic effects after hemorrhage according to studies using fixed-volume controlled blood loss models. The authors tested the null hypothesis that after uncontrolled hemorrhage there would be no difference in the hemodynamic responses between ethanol-intoxicated (EtOH+) and nonintoxicated (EtOH-) rats. METHODS: Forty Sprague-Dawley rats were anesthetized with althesin intraperitoneally. Twenty EtOH+ rats received a 3-g/kg dose of 20% ethanol intraperitoneally 60 minutes before hemorrhage. The EtOH- rats received an equivalent volume of normal saline intraperitoneally. The femoral artery was cannulated by cutdown to monitor the mean arterial blood pressure (MAP) and to obtain blood samples for lactate (LAC). Twenty rats (ten EtOH+ and ten EtOH-) underwent uncontrolled hemorrhage by 75% tail amputation. Twenty rats (ten EtOH+ and ten EtOH-) served as nonhemorrhage controls. The MAP, LAC, and cumulative hemorrhage volume were measured prehemorrhage and then every 15 minutes posthemorrhage for 120 minutes. Data were reported as mean +/- SEM. Group comparisons were analyzed by analysis of variance with repeated values and post hoc testing by Bonferroni (two tailed; alpha = 0.05). RESULTS: Initially, EtOH+ and EtOH- rats were evenly matched for LAC and MAP. The mean (+/-SD) baseline ethanol level was 170 (+/-68) mg/dL in EtOH+ rats. Cumulative hemorrhage volume was similar (p = 0.23) for the EtOH- (2.36 +/- 0.24 mL/100 g) and EtOH+ (1.87 +/- 0.32 mL/100 g) rats. No significant difference was noted in posthemorrhage MAP between EtOH- (68.6 +/- 6.8 mm Hg) and EtOH+ (69.3 +/- 7.2 mm Hg) rats (p = 1.00). The EtOH- group had a significantly higher LAC (4.94 +/- 1.07 mmol/L) than the EtOH+ group (2.27 +/- 0.59 mmol/L) (p < 0.03). CONCLUSIONS: Ethanol intoxication does not deleteriously affect the hemodynamic response to uncontrolled hemorrhage.