Biomedical subjects
Publications and source records attributed to R W Pfirrmann.
Since 1987, 80 hydroxyapatite-coated (HA) cementless total hip prostheses have been implanted. Thirty patients were examined 21 months post-operatively and the results compared with data for uncoated prosthesis. Earlier mobilisation and freedom from pain, together with evidence of bone ingrowth without connective tissue membrane formation, confirmed the benefits of HA-coated prostheses.
The NMR spectrum of taurolidine in deuterium oxide was compared with spectra obtained from model experiments with amines and formaldehyde. Head-space analysis combined with capillary GC showed that there was less than 0.004% free formaldehyde present in 2% solutions of taurolidine. This value is comparable to the concentration of formaldehyde found when the taurolidine solutions were injected directly onto GC columns.
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1 Taurolin metabolite plasma concentrations were measured in two groups of patient undergoing abdominal surgery, one group with peritonitis and the other without peritonitis, each group receiving taurolin by intraperitoneal instillation. 2 There was no significant difference in the area under the curves, for the two groups, for one of the metabolites. This would suggest that the absorption of taurolin was not modified in inflammatory conditions such as bacterial peritonitis.
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A series of derivatives of 1-(p-sulfamoyl-phenyl)-pyrrolidin-2-one were tested for anticonvulsant properties in rats and mice. The substance 1-(o-chloro-p-sulfamoyl-phenyl)-4-phenyl-pyrrolidin-2-one (1725) was found to have potent anticonvulsant activities in rats and mice against seizures induced by electroshock or pentylenetetrazol. The unsubstituted phenyl ring has to be in position 4, otherwise the activity of the product is weakened. The ortho position of the halogen atom on the N-phenyl is also important for the anticonvulsant effect; chlorine acts better than fluorine. The anticonvulsants tested also potentiate the sleeping time induced by pentobarbitone and attenuate the motor activity of mice. 1-(o-Chloro-p-sulfamoyl-phenyl)-4-phenyl-pyrrolidin-2-one (1725) has a LD50 of 1000 mg/kg p.o.; the lesser active substances generally have a LD50 greater than 5000 mg/kg p.o. Toxic effects of large doses were manifested by sedation and diarrhoea.
In view of the severe course seen in the presence of any suppurated pancreatic necrosis, it was felt to be of value to treat two patients by the adjuvant use of a new antiseptic tauroline, administered locally and, where appropriate, systemically. After surgical excision of pancreatic and peripancreatic necrotic tissue, the authors prefer to avoid active suction drainage of the residual pocket, replacing it by continuous and prolonged post-operative irrigation-lavage, together with the sequential, twice-daily use of a solution of 2 p. 100 tauroline. In view of the presence of a Gram negative septicemia (organisms identical to those of the suppurated area), the same substance was given by intravenous infusion in a 0.5 p. 100 solution, this being the only systemic, anti-infectious therapy. The effectiveness, good tolerance and originality of this new substance, active against Gram negative, Gram positive, aerobic and anaerobic organisms as well as yeast, have led the authors to immediately report their initial experience with its use.
9 derivatives of sulfanilamide were tested for anticonvulsant properties against electroconvulsive shock in mice and rats and against pentylenetetrazole shock in mice. Reference standard in these tests was sulfanilamide. Their toxic, analgesic and sedative activities were also examined. The anticonvulsive activity of sulfanilamide could be enhanced by substitution of the phenyl ring with a halogen atom. Substitution of the sulfonamide group diminishes the anticonvulsant and increases the sedative activity of sulfanilamide. Detoxication of the basic substance by substitution of the aromatic amino group only little influences the anticonvulsant activity and may even enhance it. Of the tested substances, 1742 (3-chloro-4-phenacetamido-benzene-sulfonamide) exhibited the best anticonvulsant activity; slightly weaker was PB 311 (3-chloro-4-amino-benzene-sulfonamide). The ED50 for the activity against electroconvulsive shock of both substances was about 30 mg/kg p.o. in mice. The relationship between anticonvulsant activity and inhibition of the renal and cerebral carbonic anhydrase is discussed.
A series of newly synthesized N-phenyl-substituted derivatives of succinimide were screened for anticonvulsant activity. Addition of a sulfonamide group in the p-position was of great consequence for the anticonvulsant effect. Substitution of a halogen in the m- or o-position improved activity against electroshock induced seizures. Pentylenetetrazole convulsions could only be prevented by few of these substances in smaller than 200 mg/kg oral doses. Activity could be further enhanced by adding more aliphatic or aromatic groups to the succinimide ring. The lethal doses of most of the active succinimides were higher than 5000 mg/kg p.o. With sublethal doses mice sometimes become drowsy and had myoclonic seizures and/or diarrhoea. At therapeutic dose levels kinetic disturbances, potentiation of pentobarbitone hypnosis or analgesia were rarely observed.
From a series of N-substituted hydantoin derivatives, 1-phenyl-3-(o-chloro-p-sulfonamide-phenyl)-hydantoin was found to exhibit the best anticonvulsant activity against electroshock seizures. This substance showed also a weak activity against pentylenetetrazole seizures, as well as minor analgesic and sedative effects. The toxic effects are negligible; the lethal dose in mice was higher than 5000 mg/kg p.o. The other tested hydantoin derivatives showed much weaker anticonvulsant activities.
A series of derivatives of 1-(p-sulfamoylphenyl)imidazolidinone-5 were tested for anticonvulsant properties against electroshock and pentylenetetrazole seizures. They were also screened for analgesic, sedative and toxic effects. The substances that had the best anticonvulsant activities were those with halogen substitution in the ortho position of the 1-phenylring of 1-(p-sulfamoylphenyl)-3-phenylimidazolidinone-5. Additional substitutions on the basic structure (imidazolidinone-5) or on the 3-phenylring diminished the anticonvulsant activity. The anticonvulsants are less toxic than diphenylhydantoin. Some of the substances exhibited feeble analgesic and sedative properties.
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