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The aim of this research was to evaluate the safety and reliability of an anaesthetic mixture (Equitensine: pentobarbital, chloral hydrate, dihydroxypropane, ethanol) which, unlike other 'classic' anaesthetics, such as ketamine [The Electroencephalogram in Anaesthesia, Springer, Berlin, 1984], has been demonstrated not to induce alterations in the extracellular concentrations of cerebral excitatory amino acids. Quantified EEG analysis monitoring and behavioural observation were used to quantify the degree and the time course of the changes in cerebral electrical activity, analgesia and sedation induced, in rats, by the compound under investigation. Equitensine (0.33 ml/100 g), administered intraperitoneally, induced analgesia (monitored by the tail flick method) for 60-70 min and a pattern of behavioural sedation (loss of the righting reflex) lasting, on average, 130-150 min. The EEG monitoring revealed a pattern typical of burst suppression which lasted 15-20 min, followed by another, lasting 270-300 min, characterized by slow waves of high amplitude. The quantified EEG analysis demonstrated that the changes in cerebral electrical activity lasted longer than behavioural observation suggested. The compound under examination was found to be safe, reliable and non-invasive to administer and sustain in all the animals, and quantified EEG analysis proved to be a very sensitive method for highlighting the functional changes in the central nervous system.

We have studied the kinetic constants of β;-adrenergic receptors in lymphocytes and of serotonin uptake sites in platelets from adult and elderly volunteers and from aged patients with a diagnosis of multi-infarct dementia (MID) or senile dementia of Alzheimer's type (SDAT). The results showed that in the physiological aging process, β;-adrenergic receptor density is reduced and 5HT transport system is enhanced. MID is associated to a loss of β;-adrenoceptor affinity and a slight increase in the capacity of 5HT uptake. The kinetic constants of both β;-adrenergic receptors in lymphocytes and 5HT uptake sites in platelets from SDAT patients were comparable to those observed in the adult population, being thus different from those found in the aged matched volunteers. These changes could be interpreted as resulting from compensatory mechanisms that replaced altered plasma monoamine concentrations. The apparent absence of such changes in SDAT patients could suggest the lack of these compensatory effects.