Biomedical subjects
Publications and source records attributed to S Castellani.
A case is reported in which catatonia and autonomic abnormalities occurred in a patient on long-term fluphenazine decanoate following overdose with an oral anorectic agent containing phenylpropanolamine and caffeine. The catatonic symptoms showed a rapid and complete resolution following intramuscular benztropine. A possible mechanism to explain the catatonic symptoms is discussed.
The antihypertensive activity of nifedipine in medium-term treatment has been studied in 30 patients affected by II and III WHO grade essential hypertension. After a 6-day period of placebo, patients were randomly allotted to group A (treated with single 10-mg doses of nifedipine) and group B (treated with single 20-mg doses). Treatment with nifedipine continued for 18 days. Patients in both groups were given one daily dose during the first 6 days, two daily doses in the following 6 days and three daily doses in the last 6 days. 1. Antihypertensive effect: In both groups, only three daily doses gave a satisfactory 24-hour antihypertensive activity. Nifedipine as monotherapy administered in single doses of both 10 mg (group A) and 20 mg (group B) normalized blood pressure (BP) and the measured antihypertensive effect was not statistically different in the two groups. The antihypertensive effect lasted between 7 and 8 hours after drug administration (both doses) and did not diminish with increasing duration of treatment or number of daily doses. 2. Change in heart rate: Nifedipine induced an increase in HR which diminished with shortening of the time interval between daily administrations. The effect on HR was unaltered throughout the whole experimental period. 3. Side-effects: Nifedipine did not induce orthostatic hypotension in any patient. Eleven of the 30 patients complained of side-effects, the most common being headache and palpitations. Incidence and severity of side-effects were not correlated with dose, whereas duration was longer with 20 mg. Side-effects never necessitated withdrawal of the drug.
Effects of intravenous cholinergic and dopaminergic agents on pre-cocaine olfactory bulb (OB) spindling and behavioral arousal, and on cocaine-induced OB-amygdala spindling and behavioral seizures were evaluated in seven cats with stereotaxically implanted electrodes. Spindle data were computer analyzed using a special program for spindle detection and averaging. The number, duration and amplitude of pre-cocaine OB spindles were increased by physostigmine and decreased by atropine. Physostigmine augmented pre-cocaine behavioral arousal levels and this effect was associated with the absence of cocaine seizures. Cocaine-induced amygdala spindle number was increased by physostigmine. Changes in seizure duration following cholinergic drugs suggest cholinergic inhibitory effects. These data, in accord with previous studies showing cholinergic effects on reticulocortical arousal and seizures, suggest a cholinergic mechanism which is excitatory on OB-amygdala arousal spindling and inhibitory on cocaine-induced seizures.
The influence of sympathetic stimulation (SS) (achieved by 2 min cold application) on the plasma concentration of PGE2, PGF2 alpha (radioimmunoassay), noradrenaline (NA) and adrenaline (A) (radioenzymatic assay) and on forearm vascular resistance (indirect measurement, FVR) was studied in 16 healthy volunteers before and after cyclooxygenase inhibition by indomethacin (200 mg per day orally for 3 days) and lysine acetylsalicylate (corresponding to 10 mg X kg-1 of acetylsalicylic acid -ASA- iv). SS induced a sharp increase in PGE2 (from 8.1 +/- 4.3 pg X ml-1 before SS to 23.9 +/- 6.5, P less than 0.001 2 min after the beginning of SS and then to 18.9 +/- 10.2, P less than 0.001 to 8.4 +/- 3.9, NS, 4 and 12 min respectively after the beginning of SS). Plasma levels of PGF2 alpha remained undetectable both before and after SS. The increase in PGE2 was associated with a simultaneous increase in NA (from 13.4 +/- 24.2 to 204.1 +/- 67.2 pg X ml-1, P less than 0.001 during SS and 140.6 +/- 39.5, NS at the end of the experiment), whereas A did not vary significantly. FVR increased significantly only during SS. ASA did not affect PGE2 and NA plasma levels at rest or after SS. No PGE2 was detected during IND administration either before or after SS. IND significantly increased NA plasma concentration at the observation made 12 min after the beginning of SS (185.2 +/- 64.3 pg X ml-1 vs basal values of 135.9 +/- 46.2 pg X ml-1, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Five cases are described that offer evidence for the existence of the "serotonin irritation syndrome," an anxiety state associated with high cation environments, elevated serum serotonin, and decreased urinary 5-hydroxyindoleacetic acid. The therapeutic response and reduction in serum serotonin after treatment with methysergide and/or removal from the high-cation environment support a serotonergic basis of the anxiety.
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Plasma norepinephrine (NE) and dopamine-beta-hydroxylase (DBH) activity may be altered by changes in posture, pulse rate, and BP. Twenty-three drug-free schizophrenic, ten schizoaffective, and 24 normal control subjects, and a separate group of eight schizophrenic patients treated with chlorpromazine hydrochloride and haloperidol comprised the sample. Drug-free schizophrenic patients showed higher plasma NE levels while standing and higher pulse rates when supine and standing than normal subjects. Following chlorpromazine therapy, but not following haloperidol treatment, plasma NE level increased with patients supine and standing, pulse rate increased with patients standing, and systolic BP decreased with patients standing. These findings suggest (1) a decreased peripheral alpha-adrenergic postsynaptic receptor sensitivity in schizophrenia and (2) a peripheral alpha-adrenergic blocking mechanism in chlorpromazine-induced hypotension.
The effects of naloxone, metenkephalin, and morphine were tested on phencyclidine(PCP)-induced stereotyped behaviors, ataxia, and hyperactivity in the rat. Naloxone (8 mg/kg) significantly decreased stereotypy, ataxia, and hyperactivity across all PCP doses tested (2.0, 4.0, and 6.0 mg/kg). Metenkephalin (40 micrograms/kg) and morphine (5 and 10 mg/kg) increased ataxia at the 4.0 and 6.0 mg/kg PCP doses. Stereotypy was altered by the opiates in a dose-dependent manner; enhanced by metenkephalin (40 micrograms/kg) at 2.0 mg/kg and inhibited by metenkephalin (40 micrograms/kg) and morphine (10 mg/kg) at 4.0 and 6.0 mg/kg PCP. Locomotor activity was increased by morphine (5 mg/kg) at 2 mg/kg PCP. These results suggest an involvement of central opiate receptor mechanisms in the mediation of PCP-induced behaviors in the rat.
Twenty-four patients with phencyclidine intoxication were treated with either physostigmine (2 mg i.m.) or haloperidol (5 mg i.m.) based on the presence of delusions and/or hallucinations. Several symptoms subsequently improved. Schizophreniform symptoms showed substantial improvement with haloperidol.
The authors tested the usefulness of emotional blunting as a criterion for the diagnosis of schizophrenia on 130 patients with Research Diagnostic Criteria (RDC), diagnoses of schizophrenia, schizoaffective disorder, and affective disorder, using both a scale devised by Abrams and Taylor and a global item from the Schedule for Affective Disorders and Schizophrenia. Reliability for both measures was very high. The results did not support the use of emotional blunting as a value criterion for the RDC diagnosis of schizophrenia, although it may be useful in differentiating subtypes of schizophrenia and as an exclusion criterion for affective disorders. There was no advantage in using a scale rather than a single rating measure for assigning diagnoses.
A case is presented of a 23-year-old male who displayed symptoms of manic psychosis and increased sympathetic activity following ingestion of khat (Catha edulis Forsk.). The causal role of khat was verified by visual inspection of the plant and chemical identification of phenylpropanolamine in the urine. The active constituents and possible abuse potential of khat are discussed.
A case is presented of a 31-year-old male who showed neurological and psychic symptoms following ingestion of phenylcyclohexylpyrrolidine (PHP), which was verified by identification of PHP in the urine. Treatment with physostigmine (IM) produced a rapid and sustained reversal of these symptoms.
Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
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Behavioral rating scales, developed to measure phencyclidine (PCP)-induced stereotypy and ataxia in rats, were tested using acute dose-response and chronic paradigms with concomitant assessment of locomotor activity by automated counters. Also, effects of chronic PCP on apomorphine-induced stereotypy were assessed as a test of dopamine supersensitivity. A linear dose-response effect was found for measures of all three behaviors through moderate dose levels (2-6 mg/kg), but only ataxia ratings continued to increase, showing a linear relationship through the higher (8 and 10 mg/kg) doses. Chronic daily PCP administration showed progressive augmentation of stereotypy, tolerance to ataxia at 10 min post-injection, and a biphasic increase followed by decrease to day 1 levels in locomotor activity over 14 days. No significant change was found in apomorphine stereotypy following chronic PCP treatment. The chronic behavioral changes demonstrated in this study may provide a model of PCP-induced psychological and cognitive changes seen following chronic usage in man.
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The effects of bladder distension on the production of prostaglandins (PGs) were studied in an isolated rabbit bladder preparation. Increasing bladder distensions induced a proportional release of PGs together with a parallel increase in endovesical pressure; pretreatment with indomethacin prevented both. Infusion of exogenous PGs into the arteries of bladders previously filled and treated with indomethacin produced a rise in endovesical pressure similar to that observed subsequent to distension of the untreated bladder. Our results suggest that PGs and particularly PGE2 play a role in the maintenance of vesical tone during distension.