Objective—To identify the normal gastric acid secretion
profile in dogs and determine the degree of gastric
acid suppression associated with 4 gastric acid
Animals—12 healthy Beagles.
Procedure—Intragastric pH was measured continuously
for 24-hour periods with a digital recording system
placed via a gastrostomy tube. Baseline measurements
were obtained when food was withheld
and when dogs were fed a standard diet. Dogs were
then treated with ranitidine (2 mg/kg, IV, q 12 h),
famotidine (0.5 mg/kg, IV, q 12 h), pantoprazole
(1 mg/kg, IV, q 24 h), omeprazole (1 mg/kg, PO, q 24
h), or saline solution for 7 days; intragastric pH was
recorded on days 0, 2, and 6. Subsequently, the
effects of administering famotidine (0.5 mg/kg, IV, q 8
h; 6 dogs) and omeprazole as a suspension (1 mg/kg,
PO, q 12 h; 6 dogs) were evaluated. Median 24-hour
intragastric pH, percentage of time pH was ≥ 3, and
percentage of time pH was ≥ 4 were determined.
Results—Median pH, percentage of time pH was ≥ 3,
and percentage of time pH was ≥ 4 were all significantly
higher when food was withheld than when
dogs were fed. Famotidine, pantoprazole, and
omeprazole significantly suppressed gastric acid
secretion, compared with saline solution, as determined
on the basis of median 24-hour pH and percentages
of time pH was ≥ 3 or ≥ 4. However, ranitidine
did not. Omeprazole suspension suppressed
gastric acid secretion.
Conclusions and Clinical Relevance—Results suggest
that in healthy dogs, famotidine, pantoprazole,
and omeprazole significantly suppress gastric acid
secretion. Twice daily administration of a suspension
of omeprazole, was the only regimen tested that
approached the potential therapeutic efficacy for acidrelated
disease when assessed by criteria used for
human patients. (Am J Vet Res 2005;66:425–431)
Objective—To examine cyclooxygenase (COX)
expression in canine platelets and Madin-Darby
canine kidney (MDCK) cells in culture.
Sample Population—Canine platelets and MDCK cells.
Procedure—Total RNA was recovered from isolated
canine platelets and MDCK cells. Northern blot analysis
and reverse transcription-polymerase chain reaction (RTPCR),
using complementary DNA probes and primers
designed from the human COX sequences, were used
to determine COX-1 and -2 (cyclooxygenase isoforms 1
and 2) messenger RNA (mRNA) expression.
Results—Following northern blot analysis, canine
platelets were found to express only the 2.8-kb COX-
1 transcript; COX-2 was not detected. Canine MDCK
cells expressed the 4.5-kb COX-2 transcript, in addition
to the 2.8-kb COX-1 transcript. A single DNA
band of 270 base pairs was identified following gel
electrophoresis of the product obtained from RT-PCR
of mRNA from canine platelets. Sequencing revealed
that this PCR product was 90% homologous to a portion
of the human COX-1 gene (Genbank M59979).
Conclusions and Clinical Relevance—Detection of
COX-1 by RT-PCR of RNA obtained from canine
platelets is a novel finding. The 90% homology of the
PCR product with the human sequence suggests
strong conservation between the canine and human
COX-1 gene. Cloning and sequencing of the canine
gene will be required to fully characterize homologous
regions. Because of the importance of COX in the
inflammatory process and as a potential target of currently
available nonsteroidal anti-inflammatory drugs
(NSAID), a better understanding of canine COX may
improve our ability to use NSAID appropriately,
achieve efficacy, and avoid potential adverse drug
effects in dogs. (Am J Vet Res 2000;61:1512–1516)
Objective—To determine effects of therapeutic dosages of aspirin, carprofen, deracoxib, and meloxicam on platelet function and systemic prostaglandin concentrations in healthy dogs.
Animals—10 hound-crossbred dogs.
Procedures—Aspirin (10 mg/kg, PO, q 12 h), carprofen (4.4 mg/kg, PO, q 24 h), deracoxib (2 mg/kg, PO, q 24 h), meloxicam (0.1 mg/kg, PO, q 24 h), and a placebo were administered for 7 days in a random order to each of 10 healthy dogs; there was a 21-day washout period between subsequent treatments. One-stage prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration, and plasma concentrations of thromboxane (TX)B2 and 6-keto prostaglandin (PG)F1α were measured before and after treatment administration. Platelet function was assessed by use of a platelet-function analyzer and aggregation.
Results—Aspirin, carprofen, and meloxicam did not significantly affect platelet function. Deracoxib caused a mild decrease in platelet aggregation induced by 50μM ADP. Platelet number, Hct, PT, aPTT, and plasma TXB2 and 6-keto PGF1α concentrations were unchanged after NSAID administration. Meloxicam administration resulted in a significant decrease in fibrinogen concentration, but results remained within the laboratory reference interval.
Conclusions and Clinical Relevance—Oral administration of commonly used NSAIDs at therapeutic dosages in healthy dogs did not alter plasma TXB2 and 6-keto PGF1α concentrations. Deracoxib administration resulted in a minor abnormality in platelet aggregation. Anti-inflammatory doses of aspirin did not affect platelet function as measured by use of optical aggregometry and a platelet-function analyzer. Further evaluation of the effects of aspirin and cyclooxygenase-2–selective inhibitors on hemostasis should be performed.