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  • 1
    Electronic Resource
    Electronic Resource
    Plasma concentrations of pralidoxime methylsulphate in organophosphorus poisoned patients (1992)
    Springer
    Archives of toxicology 66 (1992), S. 260-266 
    Details
    ISSN: 1432-0738
    Keywords: Pralidoxime methylsulphate ; Plasma concentration ; Organophosphorus poisoning ; Man
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using pharmacokinetic data from healthy human volunteers in a bicompartmental pharmacokinetic model, a repeated dose scheme for pralidoxime methylsulphate (Contrathion®) was developed producing plasma levels remaining above the assumed “therapeutic concentration” of 4 mg·1−1. Using the same data, it was found that a concentration of 4 mg · 1−1 could also be obtained by a loading dose of 4.42 mg · kg−1 followed by a maintenance dose of 2.14 mg · kg−1 · h−1. In order to study the pharmacokinetic behaviour of pralidoxime in poisoned patients, this continuous infusion scheme was then applied in nine cases of organophosphorus poisoning (agents: ethyl parathion, ethyl and methyl parathion, dimethoate and bromophos), and the pralidoxime plasma levels were determined. The mean plasma levels obtained in the various patients varied between 2.12 and 9 mg·1−1. Pharmacokinetic data were calculated, giving a total body clearance of 0.57±0.271· kg−1· h−1 (mean ± SD), an elimination half-life of 3.44±0.90 h, and a volume of distribution of 2.77±1.451 ·kg−1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02307171
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  • 2
    Electronic Resource
    Electronic Resource
    Plasma concentrations and haemodynamic effects of nimodipine in patients resuscitated after cardiac arrest (1989)
    Springer
    European journal of clinical pharmacology 36 (1989), S. 327-333 
    Details
    ISSN: 1432-1041
    Keywords: nimodipine ; pharmacokinetics ; haemodynamics ; cardiopulmonary resuscitation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary As the pharmacokinetics of a drug may be altered in haemodynamically compromised patients, the plasma concentrations and haemodynamic effects of the calcium entry blocker nimodipine have been examined in patients resuscitated after out-of-hospital cardiac arrest. In 7 patients nimodipine was infused at increasing rates up to 30 µg·kg−1·h−1. The plasma concentrations increased with increasing dose; at the highest dose a mean steady-state plasma concentration of 22.1 ng·ml−1 was obtained, and the mean plasma clearance was 1.4 l·kg−1·h−1. There were no marked changes in mean arterial blood pressure or heart rate. In 9 other patients nimodipine was given as a bolus infusion of 10 µg·kg−1 over 3 min, followed by a continuous infusion of 30 µg·kg−1·h−1. A mean steady-state plasma concentration of 17.6 ng·ml−1 was obtained and the mean plasma clearance was 1.9 l·kg−1·h−1. Heart rate did not change significantly, but the mean arterial blood pressure fell. The data indicate that in patients resuscitated after cardiac arrest, the pharmacokinetics of nimodipine are not markedly different from patients with other conditions, e.g. subarachnoid haemorrhage. However, if a loading dose is given to obtain a steady-state concentration sooner, there will be a fall in arterial blood pressure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00558290
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  • 3
    Electronic Resource
    Electronic Resource
    Placing obsolete hypnotics on prescription and the admission rate for acute poisoning with these drugs (1990)
    Springer
    European journal of clinical pharmacology 39 (1990), S. 519-520 
    Details
    ISSN: 1432-1041
    Keywords: Self-poisoning ; regulation ; hypnotics ; barbiturate ; OTC drugs ; prescribing practice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Since January 1 1988, certain older hypnotics have no longer been available over the counter in Belgium, but can still be dispensed on prescription. The influence of this measure on admission to our Emergency Department for acute poisoning with these hypnotics has been examined. From 1983 to 1987, a mean of 93 patients (range 87 to 99) per year were admitted as compared to 15 and 5 in 1988 and 1989, respectively. For older hypnotics that were on prescription before and after 1st January 1988, there was no decrease in 1988, and a reduction was observed in 1989. There was no change in the number of patients with benzodiazepine poisoning. The data indicate that moving these older hypnotics onto the prescription-only list resulted in a decrease in acute poisoning with them. The reduction observed in 1989 for the older hypnotics that were on prescription before as well as after 1988 may have been due to an influence of the measure on the prescribing habits of physicians.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00280947
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  • 4
    Electronic Resource
    Electronic Resource
    Cholinesterase reactivation in organophosphorus poisoned patients depends on the plasma concentrations of the oxime pralidoxime methylsulphate and of the organophosphate (1993)
    Springer
    Archives of toxicology 67 (1993), S. 79-84 
    Details
    ISSN: 1432-0738
    Keywords: Pralidoxime methylsulphate ; Organophosphorus agent ; Plasma concentration ; Cholinesterase reactivation ; Poisoning ; Man
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We measured in nine patients, poisoned by organophosphorus agents (ethyl parathion, ethyl and methyl parathion, dimethoate, or brompphos), erythrocyte and serum cholinesterase activities, and plasma concentrations of the organophosphorus agent. These patients were treated with pralidoxime methylsulphate (ContrathionR), administered as a bolus injection of 4.42 mg.kg−1 followed by a continuous infusion of 2.14 mg.kg−1/h, a dose regimen calculated to obtain the presumed “therapeutic” plasma level of 4 mg.l−1, or by a multiple of this infusion rate. Oxime plasma concentrations were also measured. The organophosphorus agent was still detectable in some patients after several days or weeks. In the patients with ethyl and methyl parathion poisoning, enzyme reactivation could be obtained in some at oxime concentrations as low as 2.88 mg.l−1; in others, however, oxime concentrations as high as 14.6 mg.l−1 remained without effect. The therapeutic effect of the oxime seemed to depend on the plasma concentrations of ethyl and methyl parathion, enzyme reactivation being absent as long as these concentrations remained above 30 μg.l−1. The bromophos poisoning was rather mild, cholinesterases were moderately inhibited and increased under oxime therapy. The omethoate inhibited enzyme could not be reactivated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01973675
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  • 5
    Electronic Resource
    Electronic Resource
    Femoral vasodilatation produced by piribedil (ET495) and its metabolite S584 in the hindleg of the dog (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 299 (1977), S. 101-103 
    Details
    ISSN: 1432-1912
    Keywords: Piribedil ; S584 ; Vasodilatation ; Haloperidol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary On local injection into the innervated hindleg of the dog piribedil, like apomorphine, produced a vasodilatation blocked by haloperidol. S584, the catechol metabolite of piribedil, produced a vasodilatation which was not blocked by haloperidol. Neither propranolol nor atropine influenced the vasodilatation produced by piribedil or S584. Denervation of the hindleg abolished the responses to piribedil and S584. During the infusion of noradrenaline into the denervated hindleg, the responses to S584 reappeared but those to piribedil did not. It is concluded from these experiments that the vasodilatation produced by piribedil in the innervated hindleg of the dog, like that of apomorphine, is mediated by dopamine receptors and that the effect of piribedil cannot be explained by the formation of its catechol metabolite S584.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508645
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  • 6
    Electronic Resource
    Electronic Resource
    Nimodipine has no beneficial effect on neurological outcome in a cardiopulmonary arrest model in the rat (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 341 (1990), S. 586-591 
    Details
    ISSN: 1432-1912
    Keywords: Cardiopulmonary arrest ; Resuscitation ; Nimodipine ; Neurological damage ; Neuronal cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Brain damage after resuscitation from cardiac arrest is believed to be related to calcium influx in ischaemic neurons and to postischaemic calcium-dependent vasospasm. We therefore evaluated the potentially protective effects of the calcium-entry blocker nimodipine in a cardiopulmonary arrest model in the rat. Male Wistar rats were anaesthetized with ketamine (group I) or hexobarbital (group II) and subjected to a KCl-induced cardiac arrest during 7 min (group I) or 12 min (group II). Five minutes after resuscitation, the rats were treated intravenously in a randomized and blind fashion. Group I received either saline or 1 μg · kg−1 · min −1 or 5 μg · kg−1 · min−1 of nimodipine and group II either saline or 1 μg · kg−1 · min−1 of nimodipine. Survival, occurrence of seizures and neurological status were assessed daily during 7 days after resuscitation. On day 7, the brains of the surviving rats were perfusion-fixed and a histopathological evaluation of the hippocampus was performed. Nimodipine, in the doses tested, had no beneficial influence on the 7 day survival rate, nor on the occurrence of seizures and the neurological and histopathological scores in the rats surviving after 7 days. With the highest dose of nimodipine, there was even a trend towards a decrease of the survival rate, probably related to the drug's hypotensive effect. Therefore, our data do not show a protective effect of nimodipine after cardiac arrest.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171740
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of dopamine and apomorphine on the response of rabbit isolated atria to sympathetic nerve stimulation (1983)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 323 (1983), S. 45-48 
    Details
    ISSN: 1432-1912
    Keywords: Prejunctional receptors ; Dopamine receptors ; Rabbit atria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In isolated rabbit atria, dopamine (10−6 M to 3×10−6 M), in the presence of cocaine and atropine, inhibits the chronotropic responses to electrical stimulation of the sympathetic nerves without influencing the responses to isoprenaline. The inhibitory effect of dopamine is antagonized by cisflupenthixol in a concentration (2.5×10−6 M) that does not antagonize the inhibitory effect of clonidine. Phentolamine, in a concentration (10−5 M) that antagonizes clonidine, does not influence the inhibitory effect of dopamine. Apomorphine (10−6 M) also produces an inhibition of the nerve stimulation-induced chronotropic responses that can be prevented by cis-flupenthixol. These data suggest that prejunctional dopamine receptors are present in rabbit atria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498826
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