The Gastroduodenal Effects of Buffered Aspirin, Carprofen, and Etodolac in Healthy Dogs

Twenty-four healthy mixed-breed dogs were divided into 4 groups. Group 1 received a placebo p.o. q12h, group 2 received an average of 16.5 (15.1-17.8) mg/kg buffered aspirin p.o. q12h, group 3 received an average of 2.2 (2.0-2.4) mg/kg carprofen p.o. q12h, and group 4 received an average of 12.8 (11.7-13.8) mg/kg etodolac p.o. q24h (with a placebo in the PM). All treatments continued for 28 consecutive days. Gastroduodenal endoscopy was performed on days -9, 0, 5, 14, and 28. Multiple gastric biopsies were obtained endoscopically on day -9 to determine each dog's Helicobacter infection status. Four regions in the stomach and 1 region in the proximal duodenum were evaluated endoscopically, and each was assigned a score from 1 to 11. Scores for each region then were summed to give a total score for each endoscopic evaluation. Erosions and submucosal hemorrhages were seen in all dogs receiving aspirin. Only minor gastric lesions were observed in the carprofen, etodolac, and control groups. No adverse clinical signs were noted in any dog given any treatment. Median total score on days 0, 5, 14, and 28, respectively, were as follows: group 1: 5.0, 5.0, 5.0, 5.0; group 2: 5.0, 27.0, 26.0, 27.5; group 3: 5.0, 5.0, 6.0, 5.0, group 4: 5.0, 7.0, 5.0, 5.0. There was no significant difference among dogs receiving carprofen, etodolac, or placebo. The administration of carprofen, etodolac, or placebo to healthy dogs resulted in significantly less gastroduodenal lesion development than in dogs receiving buffered aspirin.     

Effects of deracoxib or buffered aspirin on the gastric mucosa of healthy dogs

BACKGROUND: Use of cyclo-oxygenase-2 specific nonsteroidal anti-inflammatory drugs such as deracoxib has been advocated because of their anti-inflammatory actions and apparently low incidence of gastrointestinal adverse effects. HYPOTHESIS: Deracoxib will cause less endoscopically detectable gastric injury in dogs than aspirin, a nonselective nonsteroidal anti-inflammatory drug. ANIMALS: Twenty-four random source healthy dogs. METHODS: A randomized, placebo-controlled trial compared gastroscopic findings of dogs receiving placebo (q8h), aspirin (25 mg/kg PO q8h), or deracoxib (1.5 mg/kg QD, placebo ql2h) for 28 days. Gastroscopy on days -7, 6, 14, and 28 evaluated 4 regions of the stomach separately and visible lesions were scored. Dogs were observed every 8 hours for vomiting and diarrhea. Median total scores for each group were compared each day of endoscopic examination and total dog-days of vomiting and diarrhea were compared. Significance was determined at P < .05. RESULTS: There were significant differences in total scores of the aspirin group and both the placebo and deracoxib groups on days 6, 14, and 28. No significant differences in total scores were found between placebo and deracoxib on days 6, 14, and 28. Significant differences in dog-days of vomiting were found between the aspirin and deracoxib groups whereas no significant differences were found between the deracoxib and placebo groups. There was no detectable effect of treatment on dog-days of diarrhea. CONCLUSIONS AND CLINICAL IMPORTANCE: Administration of deracoxib to healthy dogs resulted in significantly lower gastric lesion scores, and fewer days of vomiting compared to aspirin, indicating that deracoxib is better tolerated than aspirin in some dogs.     

The effect of dosing interval on the efficacy of misoprostol in the prevention of aspirin-induced gastric injury

The effect of twice-daily administration of misoprostol on aspirin-induced gastric injury was evaluated. Twenty-four random-source dogs were divided into groups that received aspirin and misoprostol as follows: group I, aspirin 25 mg/kg PO q8h and placebo PO q8h; group II, aspirin 25 mg/kg PO q8h and misoprostol 3 microg/kg PO q8h; group III, aspirin 25 mg/kg PO q8h, misoprostol 3 microg/kg PO q12h, and placebo PO q24h; and group IV, aspirin 25 mg/kg PO q8h, misoprostol 3 microg/kg PO q24h, and placebo PO q12h for 28 days. Gastroscopy was performed on days -9, 5, 14, and 28. Visible lesions were scored on a scale of 1 (mucosal hemorrhage) to 11 (perforating ulcer). No difference in total score was identified between groups I and IV on any day. Median total scores for groups II and III were significantly (P < or = .05) lower compared to groups I and IV on day 5. Group III had a significantly lower score (P < or = .05) than groups I, II, and IV on day 28. This study suggests that misoprostol 3 microg/kg PO q12h is as effective as misoprostol 3 microg/kg PO q8h in preventing aspirin-induced gastric injury in this model. However, misoprostol 3 microg/ kg PO q8h was less effective in preventing aspirin-induced gastric injury on days 14 and 28 than in previous studies. No difference among numbers of dog-days of vomiting, diarrhea, or anorexia was detected among groups.     

Serum salicylate concentrations and endoscopic evaluation of the gastric mucosa in dogs after oral administration of aspirin-containing products

The serum salicylate concentration produced by oral administration of plain aspirin and several aspirin-containing products given at 8-hour intervals for 7 treatments was measured in 36 laboratory-conditioned adult dogs. The dogs were randomly allotted to 6 groups of 6 dogs each: group 1 was given plain aspirin at a dosage of 25 mg/kg of body weight: group 2 was given plain aspirin at a dosage of 10 mg/kg; group 3 was given buffered aspirin at a dosage of 25 mg/kg; group 4 was given enteric-coated aspirin at a dosage of 25 mg/kg; group 5 was given buffered aspirin at a dosage of 25 mg/kg; and, group 6 was given a placebo. Serum salicylate concentration was measured at 2-hour intervals for the first 8 hours, and then at 8-hour intervals for the next 40 hours. Following the last dosing, serum salicylate concentration was measured at 2-hour intervals until 56 hours; the final 2 samples were measured at 64 and 72 hours. The effect of aspirin on the gastric mucosa was studied in 12 dogs, 3 each randomly selected from groups 1, 3, 4, and 5. The gastric mucosa of each dog was examined with a fiberoptic gastroscope 3 days before the beginning of treatment; lesions were not seen. The drugs were administered as described and the gastric mucosa of each dog was reexamined at 72 hours. Administration of the aspirin-containing products at 8-hour intervals resulted in sustained therapeutic serum salicylate concentrations (greater than 5 mg/dl) in all dogs, except those of group 2. The greatest fluctuation in serum salicylate concentration was found in dogs of group 4. Gastric lesions were seen only in the 3 dogs of group 1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of deracoxib and aspirin on serum concentrations of thyroxine, 3,5,3'-triiodothyronine, free thyroxine, and thyroid-stimulating hormone in healthy dogs

OBJECTIVE: To evaluate the effects of deracoxib and aspirin on serum concentrations of thyroxine (T4), 3,5,3'-triiodothyronine (T3), free thyroxine (fT4), and thyroid-stimulating hormone (TSH) in healthy dogs. ANIMALS: 24 dogs. PROCEDURE: Dogs were allocated to 1 of 3 groups of 8 dogs each. Dogs received the vehicle used for deracoxib tablets (PO, q 8 h; placebo), aspirin (23 to 25 mg/kg, PO, q 8 h), or deracoxib (1.25 to 1.8 mg/kg, PO, q 24 h) and placebo (PO, q 8 h) for 28 days. Measurement of serum concentrations of T4, T3, fT4, and TSH were performed 7 days before treatment (day -7), on days 14 and 28 of treatment, and 14 days after treatment was discontinued. Plasma total protein, albumin, and globulin concentrations were measured on days -7 and 28. RESULTS: Mean serum T4, fT4, and T3 concentrations decreased significantly from baseline on days 14 and 28 of treatment in dogs receiving aspirin, compared with those receiving placebo. Mean plasma total protein, albumin, and globulin concentrations on day 28 decreased significantly in dogs receiving aspirin, compared with those receiving placebo. Fourteen days after administration of aspirin was stopped, differences in hormone concentrations were no longer significant. Differences in serum TSH or the free fraction of T4 were not detected at any time. No significant difference in any of the analytes was detected at any time in dogs treated with deracoxib. CONCLUSIONS AND CLINICAL RELEVANCE: Aspirin had substantial suppressive effects on thyroid hormone concentrations in dogs. Treatment with high dosages of aspirin, but not deracoxib, should be discontinued prior to evaluation of thyroid function.     

Effects of Prednisone Alone or Prednisone with Ultralow-Dose Aspirin on the Gastroduodenal Mucosa of Healthy Dogs

Background: The coadministration of prednisone and ultralow-dose aspirin has been recommended for the management of various diseases, but the safety of this combination in dogs has not been studied.
Hypotheses: The gastroduodenal lesions associated with prednisone and ultralow-dose aspirin administration will be similar to those caused by prednisone alone, but both treatments will result in more severe lesions than placebo.
Animals: Eighteen healthy adult purpose-bred dogs.
Methods: Randomized, blinded, placebo-controlled study of 3 treatment groups for 27 days: placebo, prednisone, and prednisone and aspirin. Gastroduodenoscopy was performed before and on days 5, 14, and 27 of treatment and mucosal lesions scores were assigned. Mucosal lesion scores were compared by a Kruskal-Wallis test. Clinical signs were compared by the Friedman's chi-square test (significance at P < .05).
Results: There were no significant differences in the gastroduodenal lesion scores among groups, or within groups at any time during the study. Significantly more dog-days of diarrhea occurred in the prednisone and aspirin group during treatment, compared with baseline. No significant differences in clinical signs were found among any of the groups.
Conclusion: The concurrent use of prednisone and ultralow-dose aspirin did not increase the severity of gastroduodenal lesions compared with prednisone or placebo. Coadministration of prednisone and ultralow-dose aspirin increases the frequency of mild, self-limiting diarrhea in some dogs.     

Comparison of effects of cimetidine and omeprazole on mechanically created gastric ulceration and on aspirin-induced gastritis in dogs.

A double-blind study was conducted to compare gastric ulcer healing time in nontreated dogs with that in dogs treated with either cimetidine or omeprazole. Single ulcers were created in the gastric antrum by use of a suction biopsy capsule. Each dog was given 25 mg of aspirin/kg of body weight orally for 20 days after ulcer induction. Five control dogs were given aspirin only (no anti-ulcer medication) during the 20-day study. Six dogs were given cimetidine at dosage of 10 mg/kg orally every 8 hours, and 6 dogs were given omeprazole orally at dosage of 2 mumol/kg (0.7 mg/kg) once daily. All dogs were examined endoscopically on days 5, 10, 15, and 20 and were given a score for the size of the mechanically created ulcer and a score for the degree of aspirin-induced gastritis. All dogs were euthanatized on day 21, and gastric lesions were examined histologically. Significant differences were not evident in ulcer healing scores or degree of aspirin-induced gastritis among treated and nontreated dogs on days 5, 10, 15, and 20. However, aspirin-induced gastritis was less severe in dogs of the omeprazole group than in dogs of the cimetidine or control group on each day observations were made. The effect of omeprazole given once daily was comparable with that of cimetidine given every 8 hours in lessening aspirin-induced gastritis.     

Effect of cimetidine on aspirin-induced gastric hemorrhage in dogs

Efficacy of cimetidine in the prevention of aspirin-induced gastric hemorrhage was evaluated, using 4 groups of 6 dogs given: Group 1--controls; group 2-7.5 mg of cimetidine/kg of body weight every 8 hours; group 3-7.5 mg of cimetidine/kg every 8 hours and 35 mg of nonbuffered aspirin/kg every 8 hours; and group 4-35 mg of nonbuffered aspirin/kg every 8 hours. All medication was given orally for 10 days at the time of feeding a commercial dry food. The gastric mucosa was evaluated endoscopically before treatment, on treatment day 5, and 36 hours after the final treatment. The dogs were given halothane inhalation anesthesia and were evaluated, using a grading system. Total 24-hour fecal hemoglobin (Hb) concentration was measured, using a quantitative fluorometric analysis for Hb-derived porphyrins. Control dogs and dogs given cimetidine only had no endoscopically visible gastric lesions and no increase in fecal Hb concentration. All dogs given aspirin or aspirin and cimetidine had a similar marked increase in endoscopically visible gastric hemorrhage and marked increases in fecal Hb concentration; however, there was no significant (P = 0.48) difference between the 2 groups. Seemingly, cimetidine given at an oral dosage of 7.5 mg/kg every 8 hours was not effective in preventing aspirin-induced gastric hemorrhage in clinically normal dogs.     

Renal effects of carprofen and etodolac in euvolemic and volume-depleted dogs

Objective-To determine the effects of carprofen and etodolac on renal function in euvolemic dogs and dogs with extracellular fluid volume depletion induced via administration of furosemide. Animals-12 female Beagles. Procedures-Dogs received a placebo, furosemide, carprofen, etodolac, furosemide and carprofen, and furosemide and etodolac. The order in which dogs received treatments was determined via a randomization procedure. Values of urine specific gravity, various plasma biochemical variables, glomerular filtration rate (GFR [urinary clearance of creatinine]), and renal plasma flow (urinary clearance of para-aminohippuric acid) were determined before and after 8 days of drug administration. A washout time of approximately 12 days was allowed between treatment periods. Results-Administration of furosemide, furosemide and carprofen, and furosemide and etodolac caused changes in urine specific gravity and values of plasma biochemical variables. Administration of carprofen or etodolac alone did not have a significant effect on renal plasma flow or GFR. Concurrent administration of furosemide and carprofen or furosemide and etodolac caused a significant decrease in GFR. After 12-day washout periods, mean values of GFR were similar to values before drug administration for all treatments. Conclusions and Clinical Relevance-Results indicated GFR decreased after 8 days of concurrent administration of furosemide and carprofen or furosemide and etodolac to dogs. Administration of preferential cyclooxygenase-2 inhibitors to dogs with extracellular fluid volume depletion or to dogs treated with diuretics may transiently impair renal function.     

Evaluation of adverse effects of long-term oral administration of carprofen, etodolac, flunixin meglumine, ketoprofen, and meloxicam in dogs

OBJECTIVE: To evaluate adverse effects of long-term oral administration of carprofen, etodolac, flunixin meglumine, ketoprofen, and meloxicam in dogs. ANIMALS: 36 adult dogs. PROCEDURES: Values for CBC, urinalysis, serum biochemical urinalyses, and occult blood in feces were investigated before and 7, 30, 60, and 90 days after daily oral administration (n = 6 dogs/group) of lactose (1 mg/kg, control treatment), etodolac (15 mg/kg), meloxicam (0.1 mg/kg), carprofen (4 mg/kg), and ketoprofen (2 mg/kg for 4 days, followed by 1 mg/kg daily thereafter) or flunixin (1 mg/kg for 3 days, with 4-day intervals). Gastroscopy was performed before and after the end of treatment. RESULTS: For serum gamma-glutamyltransferase activity, values were significantly increased at day 30 in dogs treated with lactose, etodolac, and meloxicam within groups. Bleeding time was significantly increased in dogs treated with carprofen at 30 and 90 days, compared with baseline. At 7 days, bleeding time was significantly longer in dogs treated with meloxicam, ketoprofen, and flunixin, compared with control dogs. Clotting time increased significantly in all groups except those treated with etodolac. At day 90, clotting time was significantly shorter in flunixin-treated dogs, compared with lactose-treated dogs. Gastric lesions were detected in all dogs treated with etodolac, ketoprofen, and flunixin, and 1 of 6 treated with carprofen. CONCLUSIONS AND CLINICAL RELEVANCE: Carprofen induced the lowest frequency of gastrointestinal adverse effects, followed by meloxicam. Monitoring for adverse effects should be considered when nonsteroidal anti-inflammatory drugs are used to treat dogs with chronic pain.     

Effects of Firocoxib and Tepoxalin on Healing in a Canine Gastric Mucosal Injury Model

Background: Little is known about the effect of dual cyclooxygenase (COX) and lipoxygenase inhibition on canine gastric mucosal healing.
Objective: This study compares the effects of putative dual COX and 5-lipoxygenase inhibition with that of COX-2 selective inhibition on gastric mucosal lesion healing in dogs.
Animals: Six normal adult mixed-breed research dogs.
Methods: Gastric body and pyloric lesions were induced by endoscopic biopsy. Dogs were treated with tepoxalin, firocoxib, or placebo for 7 days in a randomized 3-way crossover study design. Healing was evaluated on days 2, 4, and 7 of treatment by endoscopic lesion scoring. Eicosanoid concentrations in plasma and at the lesion margins were determined on days 2, 4, and 7. Repeated measures analyses were performed. All hypothesis tests were 2-sided with P < .05. Multiple comparisons were adjusted using Tukey's test.
Results: Significant treatment differences were noted in the pyloric lesion area measurements. Overall, the firocoxib group had larger lesions than the placebo ( P = .0469) or tepoxalin ( P = .0089) groups. Despite larger pyloric lesions in the firocoxib group, mucosal prostaglandin production did not differ significantly from placebo. In contrast, the tepoxalin group had significantly lower pyloric mucosal prostaglandin production compared with the firocoxib ( P < .0001) or the placebo ( P < .0001) groups but pyloric lesions were not significantly larger than those of the placebo group ( P = .7829).
Conclusion: COX-2 inhibition by firocoxib slowed wound healing by a mechanism independent of prostaglandin synthesis. Suppression of mucosal prostaglandin production by tepoxalin did not alter mucosal lesion healing compared with placebo.     

Endoscopic evaluation of the gastroduodenal mucosa following non-steroidal anti-inflammatory drug administration in the dog

The gastroduodenal mucosa of 30 healthy dogs was examined by endoscope after 7 days of oral non-steroidal anti-inflammatory drug administration. The dogs were divided into five groups. One group received ketoprofen (1 mg/kg every 24 h), one group copper-indomethacin (0.2 mg/kg every 12 h), one group 1 mg of prednisolone and 200 mg of cinchophen (1 tablet per 20 kg every 12 h), one group aspirin (15 mg/kg every 12 h) and one group gelatin (1 capsule every 12 h). Occult blood was not detected in the faeces either prior to or after non-steroidal anti-inflammatory drug administration. Packed cell volume, total plasma protein and buccal mucosal bleeding times did not significantly change after non-steroidal antiinflammatory drug administration. Gastroduodenal lesions were observed in 22 dogs. There was no significant difference in lesions between the ketoprofen, copper-indomethacin and prednisolone-cinchophen groups, but the gelatin group had significantly (p 相似文献   

Results of thyroid function tests and concentrations of plasma proteins in dogs administered etodolac

OBJECTIVE: To determine the effects of etodolac administration on results of thyroid function tests and concentrations of plasma proteins in clinically normal dogs. Animals: 19 healthy random-source mixed-breed dogs. PROCEDURE: Blood samples for measurement of serum thyroxine (T4), 3,5,3'-triiodothyronine (T3), free T4 (fT4), and endogenous canine thyroid stimulating hormone (cTSH) were measured twice before as well as on days 14 and 28 of etodolac administration (mean dosage, 13.7 mg/kg, PO, q 24 h). Plasma total protein, albumin, and globulin concentrations and serum osmolality were measured once before as well as on days 14 and 28 of etodolac administration. RESULTS: Etodolac administration did not significantly affect serum T4, T3, fT4, or cTSH concentrations or serum osmolality. Significant decreases in plasma total protein, albumin, and globulin concentrations were detected on days 14 and 28 of administration. CONCLUSIONS AND CLINICAL RELEVANCE: Results of thyroid function tests are not altered when etodolac is administered for up to 4 weeks. Therefore, interpretation of results of these tests should accurately reflect thyroid function during etodolac treatment. Plasma total protein, albumin, or globulin concentrations that are less than the respective reference range in a dog administered etodolac for > or = 2 weeks may be an effect of treatment rather than an unrelated disease process. A decrease in plasma protein concentrations may reflect subclinical injury of the gastrointestinal tract.     

In vivo effects of carprofen, deracoxib, and etodolac on prostanoid production in blood, gastric mucosa, and synovial fluid in dogs with chronic osteoarthritis

OBJECTIVE: To evaluate in vivo activity of carprofen, deracoxib, and etodolac on prostanoid production in several target tissues in dogs with chronic osteoarthritis. ANIMALS: 8 dogs with chronic unilateral osteoarthritis of the stifle joint. PROCEDURE: Each dog received carprofen, deracoxib, or etodolac for 10 days with a 30- to 60-day washout period between treatments. On days 0, 3, and 10, prostaglandin (PG) E2 concentrations were measured in lipopolysaccharide-stimulated blood, synovial fluid, and gastric mucosal biopsy specimens; PGE1 concentrations were measured in gastric mucosal biopsy specimens; and thromboxane B2 (TXB2) was evaluated in blood. RESULTS: Carprofen and deracoxib significantly suppressed PGE2 concentrations in blood at days 3 and 10, compared with baseline, whereas etodolac did not. None of the drugs significantly suppressed TXB2 concentrations in blood or gastric PGE1 synthesis at any time point. All 3 drugs significantly decreased gastric synthesis of PGE2 at day 3 but not day 10 of each treatment period. All 3 drugs decreased synovial fluid PGE2 concentrations in the affected and unaffected stifle joints at days 3 and 10. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that carprofen and deracoxib act in vivo on target tissues as COX-1-sparing drugs by sparing gastric PGE1 and PGE2 synthesis and production of TXB2 by platelets. Etodolac also appears to be COX-1 sparing but may have variable effects on COX-2 depending on the tissue. In gastric mucosa and synovial fluid, there were no significant differences in PG production between compounds at recommended concentrations.     

Multicenter randomized prospective clinical evaluation of meloxicam administered via transmucosal oral spray in client‐owned dogs

The clinical safety and efficacy of a transmucosal oral spray (TMOS) formulation of meloxicam was evaluated for the control of pain and inflammation associated with osteoarthritis in dogs. A total of 280 client‐owned dogs were enrolled at fourteen veterinary clinics: there were 187 dogs in the meloxicam TMOS group and 93 in the placebo control group. Dogs received placebo or treatment spray once daily for twenty‐eight days. Improvement in signs of osteoarthritis was measured using client‐specific outcome measures (CSOM) made at days 14 and 28 and veterinary assessments of lameness and pain on palpation made at day 28. A significantly higher number of dogs in the meloxicam TMOS group were treatment successes at 28 days (72.6%) compared with the placebo group (46.9%), based on CSOM scores. Total CSOM scores were significantly lower in the meloxicam TMOS‐treated group compared with the placebo group at both 14 and 28 days. Differences between treatment groups were not observed in veterinary assessments. Gastrointestinal effects of meloxicam were observed in some animals. Meloxicam TMOS was found to be safe and effective in dogs for the control of pain and inflammation associated with osteoarthritis.     

Superiority of the gastroduodenal safety profile of licofelone over rofecoxib, a COX-2 selective inhibitor, in dogs

This study assessed the gastroduodenal safety profile of licofelone, a new nonsteroidal anti-inflammatory drug with dual inhibitory activity against 5-lipoxygenase and cyclo-oxygenase (COX), by using endoscopic evaluations and by comparing licofelone to rofecoxib, a selective COX-2 inhibitor. Twenty-one dogs underwent blinded gastroduodenoscopies, during which the mucosa of the gastroduodenal tract was assessed and scored. Blood analyses were monitored on days 0 (baseline), 14, 28, 42, and 56. Examinations to detect fecal occult blood were performed daily. Dogs were randomly assigned to three groups that received either a placebo, licofelone at a dose of 2.5 mg/kg twice daily, or rofecoxib at a dose of 0.5 mg/kg daily, respectively. Significant differences between the groups in gastric (P = 0.003), duodenal (P = 0.009), and gastroduodenal (P = 0.002) endoscopic lesion scores were observed at day 56. Rofecoxib-treated dogs had more lesions in all areas when compared with placebo-treated dogs, more duodenal lesions when compared with licofelone-treated dogs and more lesions than they had at baseline. In contrast to licofelone, rofecoxib was found to induce significant gastric and gastroduodenal lesions in dogs that lacked pre-existing lesions at baseline. Blood analyses and fecal examinations did not reveal abnormalities in any of the experimental groups. Treatment with licofelone was well tolerated and was shown to be safer than rofecoxib in terms of upper gastrointestinal damage. In this way, this study demonstrates the gastroduodenal safety profile of licofelone for chronic treatment.     

Effects of treatment with aspirin or aspirin/dipyridamole combination in heartworm-negative, heartworm-infected, and embolized heartworm-infected dogs.

To determine the drug dose required to inhibit platelet reactivity by at least 50%, 2 drug regimens were evaluated in heartworm-negative, heartworm-infected, and heartworm-infected dogs embolized with dead heartworms. Aspirin, or a combination of aspirin and dipyridamole, were administered to 2 groups of Beagles (n = 5 each) for 5 to 9 days; a third group of 5 Beagles served as nontreated controls. For heartworm-negative dogs, mean (+/- SD) aspirin dosage that inhibited collagen-induced platelet reactivity by at least 50% was 6 (+/- 2) mg/kg of body weight given once daily. The aspirin/diphridamole combination dosage was 1 mg of each drug/kg given every 12 hours. All dogs (n = 15) were implanted with 7 adult heartworms each and remedicated (or not treated) beginning at 21 days after heartworm implantation. In heartworm-infected dogs, mean aspirin dosage required to inhibit collagen-induced platelet reactivity greater than or equal to 50% was 10 (+/- 6) mg/kg. Mean dosage of aspirin/dipyridamole combination was 1.6 +/- (0.5) mg of each drug/kg given every 12 hours. When platelet reactivity in response to collagen was determined to be inhibited by at least 50% in all medicated dogs, each dog (n = 15) was embolized with 7 dead adult heartworms to mimic heartworm adulticidal treatment. Platelet reactivity was monitored for 21 days after treatment, and drug dose was adjusted to maintain platelet inhibition by at least 50%. In embolized dogs, mean aspirin dosage was 17 (+/- 14) mg/kg given once daily. Mean dosage of the aspirin/dipyridamole combination was 2.8 (+/- 1.3) mg of each drug/kg given every 12 hours. All dogs (n = 15) were euthanatized 21 days after heartworm embolization. Each lung lobe was evaluated for severity of lesions and presence of organized or fibrinous thrombi. Lesion severity in the aspirin- and aspirin/dipyridamole-treated dogs was not significantly different from that in control dogs.     

Endoscopy of the gastroduodenal mucosa after carprofen, meloxicam and ketoprofen administration in dogs

Endoscopy was undertaken to examine the gastroduodenal mucosa of 24 healthy dogs after seven days and again after 28 days of oral non-steroidal anti-inflammatory drug (NSAID) administration. The dogs were divided into four groups. One group received ketoprofen (1 mg/kg every 24 hours), one group carprofen (2 mg/kg every 12 hours for seven days followed by 2 mg/kg every 24 hours), a third group meloxicam suspension (0·2 mg/kg every 24 hours), and the last group gelatin (one capsule every 24 hours). Serum biochemical and complete blood count parameters did not change significantly after NSAID administration. Gastroduodenal lesions were observed in 17 dogs, but in all cases these were mild to moderate. The dogs receiving gelatin or carprofen showed the fewest and the least severe lesions, although there was no statistically significant difference between the three test drugs and the control group (P 0–05). None of the dogs showed any clinical signs related to the gastrointestinal lesions.     

The glucocorticoid sparing efficacy of PhytopicaTM in the management of canine atopic dermatitis

This double-blind randomized placebo-controlled trial indicates that Phytopica™ can be an effective glucocorticoid sparing agent in canine atopic dermatitis (AD). Twenty-two dogs with perennial AD [Canine Atopic Dermatitis with Severity Index (CADESI-03) ≥ 60] were given 200 mg/kg Phytopica™ or an identical placebo in food once daily for 56 days. All dogs were initially given 0.4 mg/kg methyl-prednisolone once daily, which was then adjusted according to the daily pruritus score (0–100 mm visual analogue scale). The cumulative dose and pruritus score were lower in the Phytopica™ than the placebo group. There were statistically significant time and treatment effects for the methyl-prednisolone dose and pruritus score, but there were no significant differences between the Phytopica™ and placebo groups in the proportion of dogs that achieved a > 50% reduction in dose or pruritus scores at day 56; the mean CADESI-03 scores at days 0, 28 and 56; the numbers achieving >50% reduction in CADESI-03 at days 28 and 56; or in the owners' global efficacy score at days 28 and 56. Adverse events included diarrhoea (three Phytopica™ and one placebo treated dog), polyuria/polydipsia (three dogs in each group), and polyphagia, intermittent anorexia and panting (one dog each in the placebo group). None of these by themselves required withdrawal of treatment.     

Prevalence of gastric lesions in racing Alaskan sled dogs

Human and equine athletes are reported to have a high prevalence of gastric disease, and anecdotal evidence suggests a similar phenomenon applies to racing sled dogs. To investigate the prevalence of gastric disease in racing sled dogs, we conducted 2 gastroscopy studies on dogs competing in the annual Iditarod Sled Dog Race. A pilot study of dogs that were either dropped from the 2000 Iditarod Sled Dog Race because of illness or that finished the race indicated that, approximately 5 days after competing, 10 of 28 dogs (35%) had endoscopic evidence of gastric ulceration, erosion, or hemorrhage. The next year, an endoscopic study of 73 dogs participating in the 2001 Iditarod race was performed in order to evaluate a larger population of dogs. Data from 70 of these dogs could be used; 34 (48.5%) had ulceration, erosion, gastric hemorrhage, or some combination of these findings. When this group of 70 dogs was compared retrospectively to a control group of 87 dogs presented to the Texas A&M University (TAMU) Veterinary Medical Teaching Hospital, the Iditarod sled dogs had a significantly higher prevalence (P = .049) of gastric lesions. These findings suggest that, similar to athletes of other species, elite canine athletes have an increased prevalence of gastric disease compared to the canine population at large.