PubMed Health⌕ Search

Biomedical subjects

J Hrdlicka

Publications and source records attributed to J Hrdlicka.

At least 19 recordsLinked to original sources
PubMed1995

Disposition and urinary excretion of phenylbutazone in normal and febrile greyhounds.

Five days after the induction of acute systemic inflammation in greyhounds by intramuscular and subcutaneous injections of Freund's adjuvant, the hepatic concentrations of cytochromes P-450 and b5, the activities of the hepatic microsomal enzymes aniline p-hydroxylase and aminopyrine n-demethylase and the disposition and urinary excretion of phenylbutazone were determined. The mean plasma concentrations of phenylbutazone after intravenous administration were described by the bi-exponential equations: Cp = 144.2e-34.6t + 171.5e-0.104t for five normal greyhounds and Cp = 113.6e-16.13t + 163.1e-0.108t for five febrile greyhounds. The elimination half-lives, total body clearances and apparent volumes of distribution were 6.7 hours, 18.4 ml kg-1 hour-1 and 0.18 litre kg-1, for the normal greyhounds, and 6.4 hours, 19.5 ml kg-1 hour-1 and 0.18 litre kg-1, for the febrile greyhounds. There were no significant differences between the pharmacokinetic parameters describing the distribution and elimination of phenylbutazone, or between the quantities of phenylbutazone, oxyphenbutazone and hydroxyphenylbutazone excreted in the urine. In the febrile greyhounds, there were significant decreases in the hepatic microsomal concentrations of cytochromes P-450 and b5 and in the activities of aniline p-hydroxylase and aminopyrine n-demethylase.

Aminopyrine N-Demethylase↗
PubMed1992

Pyrrolizidine alkaloid poisoning of yaks (Bos grunniens) and confirmation by recovery of pyrrolic metabolites from formalin-fixed liver tissue.

Severe losses of yaks (Bos grunniens) were investigated in the most eastern region of Bhutan. The most serious disease was a fatal chronic skin disease with emaciation and anaemia. Post mortem examinations revealed major lesions in the liver, consisting of hepatic megalocytosis, bile duct proliferation, fibrosis and remodelling of the hepatic structure. There was also renal megalocytosis, ascites and mild to moderate icterus. Pyrrolizidine alkaloid poisoning was diagnosed and confirmed by demonstrating sulphur-bound pyrrolic metabolites of the alkaloids in preserved liver tissue. Skin lesions with hyaline parakeratosis were an important feature. Similar lesions were found in the mucosa of the oral cavity. No records could be found of such skin lesions in any other species or disease. Pyrrolizidine alkaloid poisoning seriously affects the livelihood of the local population which depends almost entirely on the yak. Various control measures are discussed. The key to be found is the identification of the toxic plants.

Animals↗
PubMed1991

[Epiglottitis and subglottic laryngitis].

Account of the course and conclusions of a working session of the Paediatric Society devoted to laryngeal obstruction in children. The participants discussed in particular the differential diagnosis of subglottic laryngitis and epiglottitis in children.

Child↗
PubMed1991

[Identification of residual antibiotics in the tissues of slaughter animals using electrophoresis bioautography].

An electrophoretic identification chart of the antibiotics penicillin, streptomycin, neomycin, erythromycin, tylosin and tetracyclines was made. Minimum inhibiting concentrations of the above antibiotics were determined for the bacterial tester-strains Bacillus subtilis BGA, Micrococcus luteus ATCC 9341 and Bacillus stearothermophillus v. calidolactis C 953. The obtained results were applied to identify residues of antibacterial substances in the tissues of slaughter animals, milk and other samples, as a follow-up of detection microbiological methods of plate agar diffusion.

Animals↗
PubMed1990

[Residues of inhibitory agents in the tissues of slaughter-house animals--comparison of microbiological methods of agar diffusion].

Three microbiological methods of agar diffusion were compared which are used to detect the residues of inhibitory substances: method using the strain Bacillus subtilis ATCC 6633 (B.s. 6633), method using the strain Bacillus stearothermophilus v. calidolactis C 953 (B. s. v. c. 953), and four-plate method. Using the compared methods, minimum inhibitory concentrations were determined for standard solutions of antibiotics and sulphadimidine. Inhibitory substances were detected parallely in the samples of the tissues of medicated and emergency-slaughtered animals, applying the three compared methods. In indicated cases inhibitory substances were identified by electrophoresis and chemical methods. The results indicate the following: 1) The B.s. 6633 method is the least sensitive of all to the residues of inhibitory substances. 2) For the purposes of detection of most antibiotics under investigation, the B.s.v.c. 953 method and the four-plate method are replaceable. The B.s.v.c. 953 method is more suitable for the detection of penicillin residues, in the case of tetracycline antibiotics it is the four-plate method. 3) Sulphadimidine residues can be detected only by the four-plate method. 4) The four-plate method enables to make the preliminary group identification of antibiotics and sulphonamides. 5) The detection limit of microbiological methods is not sufficiently sensitive to determine chloramphenicol residues; that is why the physico-chemical methods must be used.

Anti-Bacterial Agents↗
PubMed1990

A comparison of pathological changes in the mouse lung after dosing with the 3-substituted furans, myomontanone and 3-(N-ethylcarbamoyloxymethyl)furan.

Cellular changes occurring in mouse lung following the administration of myomontanone (MM) were compared with those due to another 3-substituted furan compound, 3-(N-ethylcarbamoyloxymethyl)furan (ECMF). The i.p. administration of lethal doses of these furans resulted in two different forms of lung injury. ECMF was particularly oedemagenic; it resulted in early damage to endothelial cells lining the alveolar capillaries and it also damaged the Clara cells of the terminal bronchioli. Myomontanone was much less oedemagenic and, initially, resulted in minimal cell damage. These minor changes were, however, followed by a delayed but acute injury to the type I pneumocytes, which progressed to elicit the proliferation of type II cells. These two forms of injury probably reflect significant differences in the mechanism of toxicity of the two compounds. The changes following dosing with ECMF resemble those reported after the administration of many other furans, e.g. 4-ipomeanol. The selective injury to type I pneumocytes, observed after MM, has been reported after the administration of many, apparently unrelated, compounds. The late development of MM-induced injury, long after the compound has presumably been cleared from the circulation, may result from the release of reactive metabolites which had previously been bound, reversibly, to cellular macromolecules.

Animals↗
PubMed1985

The nephrotoxicity for mice of deisopropylngaione, a minor furanoid component of toxic myoporaceous essential oils.

Deisopropylngaione (DIN) is one of a family of hepatotoxic furanosesquiterpenoid essential oils which is found in small amounts (5%) in the leaves of some specimens of the Australian plant Myoporum deserti. DIN differs from other furanoid myoporaceous essential oils in that it also causes lesions in the lungs and kidneys. At the near LD50 dose rate of 150 mg kg-1 given by intraperitoneal injection, DIN is able to cause lethal renal proximal tubular necrosis without causing significant injury to the liver and lungs in adult male mice. Following dosing, there is an increase in kidney weight due mainly to increase in water content which reaches a maximum within 16-24 h. This is accompanied by degeneration and necrosis of the proximal tubular epithelium, with proteinuria and glucosuria lasting up to 9 days in non-lethally affected mice. Marked body weight loss due to the intoxication causes a marked increase in the kidney weight:body weight ratio lasting between 9 and 18 days. Residual lesions are still present in the kidneys at 32 days, but recovery is eventually complete. DIN is structurally similar to the sweet potato toxic furan 4-ipomeanol and, like the latter, is probably injurious to the kidneys through toxic metabolism by the cytochrome-P450-containing monooxygenases of the proximal tubular epithelium. Although slight renal injury is occasionally observed in livestock poisoned by myoporaceous plants, it is unlikely that DIN is the cause. So far, DIN, like 4-ipomeanol, appears to be unequivocally nephrotoxic only for the male mouse.

Animals↗
PubMed1985

The hepatotoxicity of carbon disulphide in sheep.

Carbon Disulphide (CS2) caused liver injury when dosed orally (intraruminally) at 0.05 ml per kg body weight to overnight fasted sheep which had been given 200 mg kg-1 DDT intraruminally 1 week previously to enhance the hepatic mixed function oxygenases. The liver lesion was a periacinar hepatocellular vacuolar degeneration, fully developed at 24 h and lasting from 4 to 5 days after which the hepatic morphology returned to normal. At 24 h after dosing with CS2 there was an increase in total liver water, sodium and potassium ions but without an increase in the concentration of these cations in total liver water, and a 50% reduction in microsomal cytochrome P450 levels. Calcium concentration was either unchanged or only slightly increased. The cytoplasmic vacuoles were mainly distensions of the rough endoplasmic reticulum and contained fine amorphous or fibrillary material, probably originating from damaged smooth endoplasmic reticulum membranes. The transient influx of fluid into these organelles is thought to be due to osmotic action generated by molecules derived from the latter macromolecular membrane fragments. The lesion resembles that seen in the rat due to CS2 after pretreatment with phenobarbitone. In situations in which sheep are drenched with CS2 and CCl4 in combination, it is suggested that the development of hepatic periacinar hydropic change due to the CS2 in animals normally susceptible to CCl4 because of enhanced microsomal cytochrome P450 levels would provide a better chance of survival than if CCl4 alone was administered and extensive periacinar coagulative necrosis occurred.

Animals↗