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1.
Polymorphonuclear leukocytes (PMNLs) were isolated from an inflammatory exudate induced in the intercarpal joints of horses by an administration of carrageenin. Their superoxide production at rest and following stimulation with either serum-treated zymosan (STZ) or phorbol myristate acetate (PMA) was measured by cytochrome-c reduction. Stimulation of the cells increased the cytochrome-c reduction 10-15 times that of resting cells. The maxima were 20 nmol of reduced cytochrome-c per 10(6) cells per ml at 120 min (STZ) and 35 nmol of reduced cytochrome-c per 10(6) cells per ml at 60 min (PMA). The maximum inhibition of the cytochrome-c reduction by superoxide dismutase (Palosein) was 83.6% (STZ stimulation) and 72.1% (PMA stimulation). The non-steroidal anti-inflammatory drugs, phenylbutazone, salicylic acid, aspirin, sodium salicylate in addition to D-penicillamine and dimethylsulfoxide caused dose-dependent inhibition of the cytochrome-c reduction when the cells were stimulated by PMA. The maximum inhibitions were 64% and 36% for aspirin (10(-2) M), 32% and 17% for phenylbutazone (10(-3) M), 15% and 31% for dimethylsulfoxide (6.4 x 10(-1) M), 32% and 19% for salicylic acid (10(-2) M), 0% and 17% for sodium salicylate (10(-2) M) and 2.2% and 2.5% for D-penicillamine (10(-4) M) when the cells were stimulated by STZ and PMA, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

2.
The results showed that co-administration of either vitamin K or levamisole along with phenylbutazone abolished the latter's anti-inflammatory and antipyretic activities and reduced its analgesic effect. Prolonged administration of phenylbutazone alone to rats for 21 days increased significantly serum glutamate oxalacetate transaminase (SGOT) activity, urea and creatinine concentrations, while it decreased with significance uric acid concentration in the serum. Vitamin K, when administered together with phenylbutazone, reduced its effect on SGOT activity and creatinine concentration. Levamisole antagonised the uricosuric effect of phenylbutazone, when both were concomitantly given. Histopathological examination of the liver of rats, given phenylbutazone alone, showed mild degenerative changes, whereas in combination with levamisole these changes were exacerbated. Kidney showed oedema, degeneration, congestion, and haemorrhage. These changes were severe in rats, given phenylbutazone alone, moderate in levamisole-treated animals, and mild in those given both drugs. Combination of levamisole with phenylbutazone not only decreased the congestion of gastric mucosa but also activated the gastric glands.  相似文献   

3.
Nonsteroidal anti-inflammatory drugs are commonly used in the treatment of inflammatory conditions, and have potential value in the treatment of thrombotic disease in the horse. This study compares the potency of three nonsteroidal anti-inflammatory drugs phenylbutazone, naproxen (equiproxen) and flunixin meglumine (banamine) with respect to their effects on equine platelets. Two functional responses of horse platelets were evaluated in vitro: their ability to aggregate and their ability to make available platelet factor 3 procoagulant activity.

Flunixin at a concentration of 10-6 M significantly depressed the maximum degree of adenosine diphosphate-induced (10-6M) aggregation while much higher concentrations of phenylbutazone and naproxen (5 X 105M) were required to produce similar effects. None of the non-steriodal anti-inflammatory drugs significantly affected the duration of the lag phase or the initial velocity of adenosine diphosphate-induced aggregation within the range of drug concentrations used (10-6-10-3M). The lag phase and initial velocity of acid-soluble collagen-induced aggregation were significantly affected by 10-6 M flunixin and 10-4 M phenylbutazone or naproxen was required to produce equivalent effects. Concentrations of 5 X 10-6 M flunixin and 5 X 10-4 M phenylbutazone or naproxen were required to significantly depress the degree of collaen-induced aggregation of horse platelets.

Although the effects of the nonsteroidal anti-inflammatory drugs were qualitatively similar, flunixin was a much more potent inhibitor of platelet aggregation than either of the other two drugs (which were equipotent). At very high drug concentrations (5 X 10-4 M and greater), all three drugs produced the same degree of inhibition of equine platelet aggregation.

Platelet factor 3 activity was made available by exposing horse platelets to 10-5 M adenosine diphosphate or 1:800 acid-soluble collagen; but not by exposure to a suspension of kaolin particles. Only a small portion of the total platelet factor 3 activity was made available on stimulation with either adenosine diphosphate or collagen. Pretreatment of horse platelets with any of the nonsteroidal anti-inflammatory drugs (10-4 M concentration) had no significant effect on adenosine diphosphate or collagen-induced platelet factor 3 availability.

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4.
Turpentine-induced acute inflammatory responses in chicks were studied experimentally. Foot pad oedema was measured using a plethysmograph. Skin vascular permeability was evaluated using the Evans blue technique. Turpentine injury induced a typical biphasic response when the two parameters of the inflammatory reaction were studied. Some unexpected alterations of the turpentine-induced inflammatory response were seen when chicks received non-steroidal anti-inflammatory drugs. Pretreatment with promethazine, phenylbutazone, methysergide and indomethacin resulted in a decrease in foot oedema. An inhibitory effect upon vascular permeability was found when promethazine, phenylbutazone and indomethacin were used. Methysergide did not inhibit the increase in vascular permeability of the skin. Possible mechanisms are discussed.  相似文献   

5.
: Right dorsal colitis (RDC) is an ulcerative inflammatory bowel disorder of the horse that has been associated with the administration of non-steroidal anti-inflammatory drugs (NSAIDs), particularly in horses treated when dehydrated or toxaemic. The acute form of RDC may result in profuse diarrhoea, severe colic, dehydration, endotoxic shock and even death; the chronic form may be manifest by mild to moderate intermittent colic, ventral oedema and weight loss with or without diarrhoea. The most consistent laboratory findings are anaemia, hypoproteinaemia, hypoalbuminaemia and hypocalcaemia. Medical management of RDC requires avoidance of NSAIDs, of stressful experiences and of large-volume diets. Specific medications such as sucralfate and metronidazole have been used to treat RDC in the horse. The use of dietary additions such as psyllium and corn oil has been mentioned in the literature.RDC has not been reported previously in Ireland or Britain; here we report that the condition was diagnosed in three horses in Ireland on the bases of a history of phenylbutazone therapy, clinical signs, clinical pathology and ultrasonography. In two of the three horses the diagnosis was confirmed by direct inspection of the affected colon at celiotomy.  相似文献   

6.
The disposition kinetics and systemic availability of nonsteroidal anti-inflammatory (NSAI) agents as well as their antipyretic and anti-nociceptive properties are reviewed in different species. The anti-inflammatory versus bradykinin, serotonin and kaolin oedema activities of aspirin (ASA), phenylbutazone (PBZ) and indomethacin (IDM) explain their large use in veterinary medicine. The low analgesic effect versus NO3Ag arthritis, radiant heat and tail pressure of indomethacin and oxyphenbutazone contrasts with the widespread activity of phenazone. The comparative inhibitory effect of NSAI agents on the rat fundus contraction due to arachidonic acid is an indication of their relative inhibition of prostaglandin biosynthesis. Among the side-effects of NSAI agents, the long-lasting hyperactivity and hypomotility induced by a parenteral injection of phenylbutazone in the dog is of importance despite the fact that in this species, as in the horse, the average half life is only 6 h due to side-chain hydroxylation (versus 42 h in man for whom conjugation is a major pathway). Initiation of therapy with a loading dose followed by maintenance doses (each half the size of the loading dose) at constant intervals equal to the half-life of the drug has been shown to be suitable for most drugs with long half-life values. According to this a tentative harmless dosage regimen can be calculated for NSAI therapy in different species.  相似文献   

7.
Injuries sustained by horses during racing have been considered as an unavoidable part of horse racing. Many factors may be associated with the musculoskeletal injuries of Thoroughbred race horses. This study surveyed the amounts of nonsteroidal anti-inflammatory agents (NSAIDs) in injured horse's biological system (plasma) at Kentucky racetracks from January 1, 1995 through December 31, 1996. During that period, there were 84 catastrophic cases (euthanized horses) and 126 noncatastrophic cases. Plasma concentrations of NSAIDs were determined by High Performance Liquid Chromatography in injured and control horses. The possible role of anti-inflammatory agents in musculoskeletal injuries of Thoroughbred race horses was investigated by comparing the apparent concentrations of NSAIDs in injured horses to concentrations in control horses. The plasma concentrations of phenylbutazone and flunixin were higher in injured horses than in control horses. Most injured and control horses did not have a detectable level of naproxen in their plasma samples. Further studies must be carried out to determine whether horses with higher plasma concentrations of NSAIDs have an altered risk of musculoskeletal injuries compared with other horses.  相似文献   

8.
In equids, phenylbutazone at high doses induces gastric disease, primarily in the glandular portion of the stomach. However, the mechanism of nonsteroidal anti‐inflammatory drug (NSAID)‐induced gastric disease in horses has yet to be determined. While phenylbutazone‐associated ulceration is often attributed to a decrease in basal gastric prostaglandins, this has not been demonstrated in the horse. Twelve horses were randomly assigned to treatment (n  = 6; 4.4 mg/kg phenylbutazone PO in 20 ml molasses q 12 hr for 7 days) or placebo (n  = 6; 20 ml molasses PO q 12 hr for 7 days) groups. Before treatment and 3 and 7 days after initiation of treatment, gastroscopy was performed and glandular gastric biopsies were collected and frozen at ?80°C. Glandular disease was assessed on a scale of 0–4. Prostaglandin E2 concentrations in biopsies were measured using a commercially available enzyme‐linked immunosorbent assay. All phenylbutazone‐treated horses developed grade ≥2 glandular disease. Prostaglandin concentrations increased over time (p  = .0017), but there was no effect of treatment (p  = .49). These findings indicate that despite induction of glandular disease grade ≥2, phenylbutazone did not decrease basal glandular gastric prostaglandin E2 concentration.  相似文献   

9.
Four cases of ulceration and stricture of the right dorsal colon were encountered. Ulceration of the right dorsal colon is generally associated with nonsteroidal anti-inflammatory drug (NSAID) toxicosis but there are few reports of stricture following ulceration. All four horses had recent phenylbutazone use: three had been given doses well in excess of the recommended dose and in one the dose was marginally above those recommended but was combined with administration of other NSAIDs. All four horses presented with intermittent low-grade colic, weight loss and ventral oedema. Diarrhoea was also seen in three of them. All had hypoproteinaemia due to severe hypoalbuminaemia, and hyperfibrinogenaemia. Hypoalbuminaemia was less severe in one horse and this horse was successfully managed medically. Two cases were definitively diagnosed at exploratory celiotomy and two at necropsy. Exploratory celiotomy was performed in two horses: one was euthanased at surgery and one was managed successfully with medical treatment and remained normal 1 year after surgery. Medical management included feeding of a low-roughage pelleted ration, corn oil, psyllium mucilloid, and discontinuation of NSAID administration.  相似文献   

10.
The clinically recommended dose rate of phenylbutazone (4.4 mg/kg) was administered intravenously as a single dose to five Welsh Mountain ponies. Distribution of phenylbutazone and its active metabolite oxyphenbutazone into body fluids was studied by measuring concentrations in plasma, tissue-cage fluid, peritoneal fluid and acute inflammatory exudate harvested from a polyester sponge model of inflammation. The ready penetration of phenylbutazone into inflammatory exudate was demonstrated by the relatively high mean value for Cmax of 12.4 μg/ml occurring at a time of 4.6 h and a mean AUQ)_24 of 128 μg-h/ml. A high mean exudate: plasma AUCo_24 ratio of 0.83 was recorded. Plasma: exudate concentration ratios for phenylbutazone were initially greater than and subsequently less than one; the slower clearance from exudate was indicated by approximate t½β values of 4.8 and 24 h for plasma and exudate, respectively. These findings may help to explain the relatively long duration of action of phenylbutazone, in spite of a plasma elimination half-life of less than 5 h. Lower values of Cmax and AUC0–24 for phenylbutazone passage into peritoneal fluid (6.3 μg/ml and 45 (μh/ml) were recorded, and a limited number of sampling times indicated a similar degree of penetration as into tissue cage fluid. Mean concentrations of oxyphenbutazone in all fluids were lower than phenylbutazone concentrations at all times, but ready penetration of the metabolite into body fluids, especially into inflammatory exudate, occurred suggesting that oxyphenbutazone may contribute to the anti-inflammatory effect. The hyperaemia of acute inflammation and the high protein levels in inflammatory exudate may both assist passage of phenylbutazone and oxyphenbutazone into exudate. The slower clearance of both compounds from exudate, periton?ceal fluid and tissue cage fluid than from plasma is similar to previous reports for other drugs.  相似文献   

11.
OBJECTIVE: To determine the effectiveness of administering multiple doses of phenylbutazone alone or a combination of phenylbutazone and flunixin meglumine to alleviate lameness in horses. ANIMALS: 29 adult horses with naturally occurring forelimb and hind limb lameness. PROCEDURES: Lameness evaluations were performed by use of kinematic evaluation while horses were trotting on a treadmill. Lameness evaluations were performed before and 12 hours after administration of 2 nonsteroidal anti-inflammatory drug (NSAID) treatment regimens. Phenylbutazone paste was administered at approximately 2.2 mg/kg, PO, every 12 hours for 5 days, or phenylbutazone paste was administered at approximately 2.2 mg/kg, PO, every 12 hours for 5 days in combination with flunixin meglumine administered at 1.1 mg/kg, IV, every 12 hours for 5 days. RESULTS: Alleviation of lameness was greater after administration of the combination of NSAIDs than after oral administration of phenylbutazone alone. Improvement in horses after a combination of NSAIDs did not completely mask lameness. Five horses did not improve after either NSAID treatment regimen. All posttreatment plasma concentrations of NSAIDs were less than those currently allowed by the United States Equestrian Federation Inc for a single NSAID. One horse administered the combination NSAID regimen died of acute necrotizing colitis during the study. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of a combination of NSAIDs at the dosages and intervals used in the study reported here alleviated the lameness condition more effectively than did oral administration of phenylbutazone alone. This may attract use of combinations of NSAIDs to increase performance despite potential toxic adverse effects.  相似文献   

12.
Biochemical and haematological effects of phenylbutazone in horses   总被引：1，自引：0，他引：1  
Five matched pairs of horses were used to investigate the effects of phenylbutazone on a range of physiological, biochemical and haematological variables. The drug was given by mouth daily for 15 consecutive days at the manufacturer's recommended dose rates to one group of horses (Group A); the second group (Group B) received equivalent doses of a placebo. For some of the measured parameters, significant changes were recorded in both groups, indicating background instability. Significant decreases in serum total protein, albumin, plasma pH, viscosity and magnesium, and an increase in albumin: globulin ratio occurred in Group A, but not in Group B. These changes were, therefore, attributed to phenylbutazone or its metabolites. Toxicologically, the change in pH is probably unimportant but the decrease in protein concentration may have resulted from a protein losing enteropathy and/or from decreased synthesis in the liver. In one animal which received phenylbutazone, clinical signs of toxicity (lethargy, inappetence, oedema) were observed and evidence of hepatotoxicity and haematological changes were also noted in this horse. It is concluded that recommended dose rates of phenylbutazone should never be exceeded and that the period for which the highest dose (4.4 mg/kg body weight twice daily for four days) is administered should be reduced. In clinical cases, where phenylbutazone toxicity is suspected, measurement of serum or plasma protein concentration might provide an indication of the need to reduce dose levels or stop therapy.  相似文献   

13.
The pharmacokinetics of the two active anti-inflammatory compounds, isopropylaminophenazone and phenylbutazone, were investigated in the horse. Therapeutic intravenous doses of 12 mg/kg body weight and 6 mg/kg body weight, respectively, were given separately and as a combination to five horses. Blood concentrations were described by two-compartment kinetics. Significantly lower total clearances, unchanged volumes of distribution, and hence significantly higher elimination half-lives were found for both substances when administered as a combination. It is possible that the hydroxylated metabolites of the substances are responsible for the presumed metabolic interference.  相似文献   

14.
Nonsteroidal anti-inflammatory drugs impair platelet aggregation and secretion in man, pigs, and rabbits and inhibit platelet thromboxane/prostaglandin synthesis. The present investigation studied the effects of phenylbutazone on platelet aggregation and bleeding times in the horse. Aggregation responses to adenosine diphosphate and collagen were markedly impaired 15 minutes and 2 hours after treatment, but 4 hours after treatment, platelet responses approximated those prior to treatment. The in vivo effect of phenylbutazone correlated with its plasma concentrations. Phenylbutazone, like aspirin, appeared to exert its effect by inhibiting thromboxane/prostaglandin synthesis, because thrombin-induced malondialdehyde formation was inhibited. However, unlike aspirin, free arachidonate-induced malondialdehyde synthesis was reduced but not eliminated, which suggested that phenylbutazone may have more than one site of action. Although collagen-induced platelet aggregation was impaired, a response was still present, and bleeding times were not altered by phenylbutazone treatment. To account for these findings, it is proposed that equine platelets can respond to collagen by thromboxane/prostaglandin independent pathways. The physiologic and pathophysiologic importance of these findings is discussed.  相似文献   

15.
Tissue irritation after intramuscular injections of 4 nonsteroidal anti-inflammatory agents was studied in 5 lactating cows. Preparations containing phenylbutazone, flunixin, metamizole (dipyrone) and ketoprofen were investigated; physiological saline was used as a control substance. Tissue reactions at the injection sites were examined by palpation and by determining serum creatine kinase. A kinetic method based on creatine kinase released from the injured muscle tissue was used, which allowed estimation of the amount of damaged muscle. The metamizole preparation clearly provoked signs of pain all the cows. After flunixin and phenylbutazone injections slight reactions were observed, and ketoprofen and saline did not cause any clinical signs. Some palpatory findings after injections were found for all the preparations except saline. Based on serum creatine kinase, the 2 most irritating preparations were the ones containing flunixin and phenylbutazone. After injections of these 2 substances, the estimated amount of damaged muscle was about 80 grams. The statistical difference between flunixin and phenylbutazone and the other 2 preparations was significant. Physiological saline had no effect on serum creatine kinase. For preparations containing phenylbutazone and flunixin, intravenous administration is recommended.  相似文献   

16.
Landuyt, J., Delbeke, F.T. & Debackere, M. The intramuscular bioavailability of a phenylbutazone preparation in the horse.J vet. Pharmacol. Therap. 16, 494– 500.
The plasma concentrations of phenylbutazone (PBZ) and its major metabolites, oxyphenbutazone (OPBZ) and γ-OH-phenylbutazone (OHPBZ) were determined for up to 72 h in six horses, following intravenous (i.v.) and intramuscular (i.m.) administration of 4 g phenylbutazone, 20 ml Phenylarthrite® Ventoquinol (Vetoquinol Specialites Pharmaceutiques Veterinaires, Magny-Vernois, 70200 Lure, France). After i.v. dosing the plasma disposition was best described by a two-compartment open model. The hydroxylated metabolites OPBZ and OHPBZ were present in detectable concentrations for 72 h and 48 h, respectively. After 36 h the OPBZ concentrations exceeded plasma PBZ concentrations. The plasma disposition following i.m. injection could be described by a one-compartment open model. The hydroxylated metabolites OPBZ and OHPBZ were present in detectable concentrations for 72 h and 36 h, respectively. Only after 72 h was the concentration of OPBZ in plasma higher than the concentration of PBZ. The mean i.m. bioavailability of phenylbutazone was calculated to be 91.7 ± 10.1%.  相似文献   

17.
The dose-related effects of phenylbutazone and Depo-Medrol® on chondrocyte viability and chondrocyte-mediated synthesis and depletion of proteoglycans were investigated using cultured explants of equine middle carpal joint articular cartilage. Explants from 12 horses (941 × 3 mm diameter) were cultured for a total of 5 days, which included 3 days' exposure to either phenylbutazone (0, 2, 20, 200 or 2000 μg/mL) or Depo-Medrol (0, 20, 200 or 2000 μg/mL). For each explant, amino sugar content was used as a measure of proteoglycan content, 35S incorporation as a measure of the rate of proteoglycan synthesis and the number of pyknotic nuclei as a measure of cell death. During culture, control explants remained metabolically active and viable but suffered a net loss of proteoglycans. Proteoglycan loss was reduced by the presence of either phenylbutazone or Depo-Medrol. This effect was significant at clinically relevant concentrations of phenylbutazone (2–20 μg/mL), but not Depo-Medrol (20–200 μg/mL). Depo-Medrol caused a dose-dependent suppression of proteoglycan synthesis at all concentrations, but chondrocyte viability was affected only at the 2000 μg/mL dose. Phenylbutazone affected proteoglycan synthesis and cell viability only at the 2000 μg/mL concentration. At all concentrations, the anticatabolic effects of each drug influenced the proteoglycan content of the explants far more than did any antianabolic or cytotoxic drug effect. The results suggest that the therapeutic potential of both phenylbutazone and Depo-Medrol may not be restricted to their anti-inflammatory effects on the soft tissues of the joint.  相似文献   

18.
Experiments to determine the residual plasma concentrations of phenylbutazone and its metabolites found in horses racing on a 'no-race day medication' or 24-h rule were carried out. One dosing schedule (oral-i.v.) consisted of 8.8 mg/kg (4 g/1000 lbs) orally for 3 days, followed by 4.4 mg/kg (2 g/1000 lbs) intravenously on day 4. A second schedule consisted of 4.4 mg/kg i.v. for 4 days. The experiments were carried out in Thoroughbred and Standardbred horses at pasture, half-bred horses at pasture, and in Thoroughbred horses in training. After administering the i.v. schedule for 4 days to Thoroughbred and Standardbred horses at pasture, the mean plasma concentrations of phenylbutazone increased from 0.77 microgram/ml on day 2 to 2.5 micrograms/ml on day 5. The shape of the frequency distribution of these populations was log-normal. These data are consistent with one horse in 1,000 yielding a plasma level of 8.07 micrograms/ml on day 5. After administration of the oral-i.v. schedule to Thoroughbred and Standardbred horses at pasture, the mean plasma concentrations of phenylbutazone were 3.4 micrograms/ml on day 2 and 3.5 micrograms/ml on day 5. The range on day 5 was from 1.4 to 8.98 micrograms/ml and the frequency distribution was log-normal. These data are consistent with one horse in 1000 having a plasma level of 15.8 micrograms/ml on day 5. In a final experiment, the oral dosing schedule was administered to 62 Thoroughbred horses in training. Plasma concentrations on day 5 in these horses averaged 5.3 micrograms/ml. The range was from 1.3 to 13.6 micrograms/ml and the frequency distribution was log-normal. Statistical projection of these values suggests that following this oral dosing schedule in racing horses about one horse in 1000 will yield a plasma level of 23.5 micrograms/ml of phenylbutazone 24 h after the last dose.  相似文献   

19.
An acute phase reaction was elicited in four horses to which Freund's adjuvant was administered intramuscularly. The localised inflammation was accompanied by changes in the plasma concentrations of copper, iron and zinc. The plasma copper concentration, the plasma ceruloplasmin copper concentration and the ceruloplasmin oxidase activity in the plasma steadily increased to a maximum 24 days after the administration of the adjuvant. At this time, the plasma copper concentration was 2.2 micrograms/ml, a 90 per cent increase over the baseline concentration. The ratio of the concentration of plasma ceruloplasmin copper to plasma copper remained constant, indicating that the non-ceruloplasmin bound copper component of the plasma is also an acute phase reactant in the horse. The plasma zinc and iron concentrations decreased to 59 per cent and 30 per cent of their respective baseline concentrations and the severity of the inflammation appeared to influence the plasma concentrations of each metal. Weak correlations between the plasma fibrinogen concentration and the plasma copper and zinc concentrations of 25 horses with plasma fibrinogen concentrations of 5 g/litre or greater indicated that a single measurement of plasma copper concentration is not useful in the diagnosis of non-specific inflammatory disorders of the horse. However, the results suggest that the plasma copper concentrations in serial samples may be used to monitor the resolution of inflammatory disorders in the horse.  相似文献   

20.
The direct effects of four non-steroidal anti-inflammatory drugs (NSAIDs) on equine polymorphonuclear (PMN) and mononuclear (MN) leucocyte movement were investigated using two in vitro assay systems. The Boyden chamber microfilter technique measures both chemokinetic and chemotactic locomotion, and the agarose microdroplet assay measures solely chemokinesis. Zymosan-activated plasma (ZAP) and the synthetic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) were used as standard chemoattractants for PMN and MN leucocytes, respectively. The actions of six concentrations of each NSAID, indomethacin (50 microM-10 mM), phenylbutazone (10 microM-1 mM), oxyphenbutazone (2.5 microM-500 microM) and flunixin (0.1 microM-50 microM), in suppressing cell movement induced by ZAP and FMLP were investigated. All four drugs exerted inhibitory effects on induced movement of both cell types in the Boyden chamber assay, usually in a concentration-dependent manner, although oxyphenbutazone action on PMN cells occurred only at the highest concentration tested. Significant inhibition of PMN and MN cell locomotion was produced by indomethacin, flunixin and oxyphenbutazone, and inhibition of PMN movement by phenylbutazone occurred in the agarose microdroplet assay. Flunixin was the most potent of the four drugs investigated in both assay systems. The findings may be of importance to the use of phenylbutazone and flunixin as NSAIDs in equine medicine, since the concentrations used were similar to concentrations of both drugs and the phenylbutazone metabolite oxyphenbutazone previously reported to occur in equine plasma and inflammatory exudate.  相似文献   

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