The major problems of racing in the United States at the present time are caused by too much racing. This has led to too few horses and small fields. Consequently many owners and trainers are trying to enter their horses too frequently and to race them when they are not really fit to run. The desire to race horses as frequently as possible has led to constant pressure from horsemen through their organizations for so called "permissive medication". Started in the state of Colorado approximately ten years ago this has grown until finally there are only a few states, notably New York and New Jersey that have resisted the pressure. The drug that gave the opening wedge to permissive medication was phenylbutazone, but this in many states has led to the inclusion of other drugs including analgesics and drugs that veterinarians claim are needed for therapeutic purposes. Some states have endeavoured to control phenylbutazone medication by quantitation and while lower limits cause little difficulty, maximum allowable limits have caused problems and are not practical. While there has been no publicity to my knowledge about frusemide (furosemide, lasix) the abuse of this drug for so called "bleeders" is an example that may seriously interfere with drug detection in urine and its use should be confined to proven "bleeders" (i.e. horses suffering from epistaxis). Pre-race blood testing began roughly ten years ago at the harness tracks and has been resisted by our flat tracks rather successfully up to the present time. The blood testing methods and those used by the same laboratories in post-race urine testing is inadequate and will not detect many illegal drugs. (+info)
Anti-ulcer effects of 4'-(2-carboxyetyl) phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride (cetraxate) on various experimental gastric ulcers in rats.
Anti-ulcer effects of cetraxate, a new compound possessing anti-plasmin, anti-casein and anti-trypsin actions were investigated by using experimental gastric ulcer models in rats. Cetraxate, 300 mg/kg p.o. showed significant inhibitory effects of 65.3%, 70.0%, 30.2%, and 67.1% against aucte types of ulcers producing by aspirin, phenylbutazone, indomethacin, and pyloric ligature (Shay's ulcer), respectively. These effects were greater than those obtained by gefarnate and aluminum sucrose sulfate may be mainly attributed to the protecting action of this drug on gastric mucosa. Ctraxate further revealed remarkable inhibitory effects on chronic types of ulcers produced by acetic acid, clamping, and clamping-cortisone. In acetic acid ulcer in particular, cetraxate was found to have a dose-dependent inhibitory effect at doses over 50 mg/kg. Of test drugs including L-glutamine and methylmethionine sulfonium chloride, cetraxate showed the most remarkable inhibitory effect on beta-glucuronidase activity in ulcer tissue of these three types of ulcers. These findings suggest that cetraxate may prevent the connective tissue in the ulcer location from decomposition due to lysosomal enzymes such as beta-glucuronidase, thereby accelerating the recovery from ulcer. (+info)
The effect of streptomycin, oxytetracycline, tilmicosin and phenylbutazone on spermatogenesis in bulls.
To determine whether declining semen quality associated with health problems may be due to certain antibiotic or anti-inflammatory treatments, semen was collected 3 times per week for up to 42 d from 6 normal bulls after treatment with oxytetracycline, tilmicosin, dihydrostreptomycin, or phenylbutazone. No adverse effects on semen quality were observed. (+info)
Antinative DNA antibodies as a reaction to pyrazole drugs.
A case history is presented of the occurrence of a high binding capacity for native DNA in the serum of a patient on phenylbutazone. This reverted to normal on stopping the drug. The patient also had a reversible neutropenia and leucopenia, and it is suggested that the high anti-DNA binding capacity was a feature of a drug-induced lupus-like phenomenon. (+info)
Effect of 1-(m-chlorophenyl)-3-N,N-dimethyl-carbamoyl-5-methoxypyrazole (PZ-177) on drug-metabolizing enzyme on rat liver.
Effect of 1-(m-chlorphenyl)-3-N,N-dimethylcarbamoyl-5-methoxypyrazole (PZ-177) (62.5 and 250 mg/kg) on rat liver was investigated by measuring liver weight and drug-metabolizing enzyme activity. The effects of PZ-177 were compared with those of phenobarbital, phenylbutazone, and tiaramide hydrochloride. Increase of liver weight and liver/body weight ratio was observed in the rats treated with PZ-177 or phenobarbital, however, normal values were reverted to 1--2 weeks after treatment. PZ-177 similar to phenobarbital, significantly enhanced the activity of aminopyrine demethylase and aniline hydroxylase after 1,2, and 4 weeks of treatment. In contrast, tiaramide hydrochloride decreased the activity of aminopyrine demethylase and aniline hydroxylase after 1 week of treatment, and significantly enhanced the activity of these enzymes after 4 weeks. The content of cytochrome P-450 and the activity of NADPH cytochrome C reductase were also increased by treatment with PZ-177. The sleeping time by hexobarbital was shortened significantly by the administration of PZ-177. Vmax for both aminopyrine demethylase and aniline hydroxylase increased by treatment with PZ-177. However, only the Km for aniline hydroxylase was increased by treatment with PZ-177. From the results of these experiments, PZ-177 may be classified as a phenobarbital-type inducer. (+info)
Feprazone, a new anti-inflammatory agent. Studies of potency and gastrointestinal tolerance.
Two studies are reported; a double-blind cross-over trial of feprazone 600 mg daily and aspirin 3.6 g daily in the treatment of rheumatoid arthritis, and an uncontrolled open study of gastrointestinal tolerance in twenty rheumatoid arthritis patients with known intolerance to other drugs. The first study showed that feprazone was significantly superior to aspirin in all the parameters tested. In the second study all twenty patients showed an improvement of their gastrointestinal symptoms, nineteen reporting no symptoms at all when taking the new preparation. (+info)
Reiter's disease in three boys.
Three cases of Reiter's disease occurring in boys under the age of 16 are reported. One of these presented with a Salmonella enteritidis diarrhoea. This conforms to the 'dysenteric' form of Reiter's disease usually seen in Europe and rarely reported in England. Another presented with a monarticular arthritis of the knee, and the third has developed a chronic relapsing erosive arthritis as a result of sexually acquired Reiter's disease--an occurrence not previously reported in this age group. We draw attention to the frequency of diarrhoea in these children and the sex incidence of 1 female to 4--5 males, which agrees more with Reiter's disease of dysenteric origin than that acquired venereally. (+info)
Molecular characteristics of the inhibition of human neutrophil elastase by nonsteroidal antiinflammatory drugs.
Nonsteroidal antiinflammatory drugs(NSAIDs) are known as clinically effective agents for treatment of inflammatory diseases. Inhibition of cyclooxygenase has been thought to be a major facet of the pharmacological mechanism of NSAIDs. However, it is difficult to ascribe the antiinflammatory effects of NSAIDs solely to the inhibition of prostaglandin synthesis. Human neutrophil elastase (HNElastase; HNE, EC 22.214.171.124) has been known as a causative factor in inflammatory diseases. To investigate the specific relationship between HNElastase inhibition and specificity of molecular structure of several NSAIDs, HNElastase was purified by Ultrogel AcA54 gel filtration, CM-Sephadex ion exchange, and HPLC (with TSK 250 column) chromatography. HNElastase was inhibited by aspirin and salicylate in a competitive manner and by naproxen, ketoprofen, phenylbutazone, and oxyphenbutazone in a partial competative manner, but not by ibuprofen and tolmetin. HNElastase-phenylbutazone-complex showed strong Raman shifts at 200, 440, 1124, 1194, 1384, 1506, and 1768 cm(-1). The Raman bands 1194, 1384, and 1768 cm(-1) may represent evidences of the conformational change at -N=N-phi radical, pyrazol ring, and -C=O radical of the elastase-drug complex, respectively. Phenylbutazone might be bound to HNElastase by ionic and hydrophobic interaction, and masked the active site. Inhibition of HNElastase could be another mechanism of action of NSAIDs besides cyclooxygenase inhibition in the treatment of inflammatory diseases. Different inhibition characteristics of HNE-lastase by NSAIDs such as aspirin, phenylbutazone-like drugs and ineffective drugs could be important points for drawing the criteria for appropriate drugs in clinical application. (+info)