Development of gastroscopic food sensitivity testing in dogs.

The aims of this study were to develop a gastroscopic food sensitivity testing (GFST) technique for clinical use in dogs and to determine if the results of GFST were influenced by the feeding of a hypoallergenic diet immediately before the testing period ("unmasking"). The technical requirements for GFST were devised during a total of eight endoscopies performed in four healthy dogs. GFST was performed in anesthetized dogs in sternal recumbency. Food extracts were dripped onto the dependent aspect of the body of the stomach via plastic tubing passed through the endoscope. Changes were observed within 2 to 3 minutes of application, and included localized mucosal swelling and erythema, generalized mucosal erythema, and hyperperistalsis. The influence of "unmasking" was then examined in 6 atopic and 2 healthy dogs, which underwent GFST on three occasions, 4 weeks apart. Before the first and third testing periods, the dogs consumed a commercial dry dog food. For 5 days before the second testing period the dogs were fed a hypoallergenic elemental diet. Oral challenges were performed to identify which of the dogs had clinically overt immediate food sensitivity. Localized swelling was most frequently correlated with positive challenge PO. No positive reactions occurred in response to the negative control extract (lamb). The number of positive GFST results increased after feeding the hypoallergenic diet. In conclusion, these preliminary results indicate that GFST holds substantial promise for the diagnosis of immediate food sensitivities affecting the gastrointestinal tract. The sensitivity of the procedure appears to be enhanced by preceding testing with a hypoallergenic diet.

Changes in cerebrospinal fluid and plasma amino acid concentrations with elevated dietary protein concentration in dogs with portacaval shunts.

Effects of dietary protein concentration on plasma and cerebrospinal fluid (CSF) amino acids (AA) in dogs with portacaval shunts (PCS) were examined. An 18% protein purified diet (18P) was fed to 4 PCS dogs and 2 controls; at week 10, 2 of the PCS dogs were switched to 36% protein (36P) until week 28. Effects of the diet switch on plasma and CSF AA in 8 normal dogs were determined in another experiment. Neither surgery nor protein level significantly affected average food intake (weeks 10-28). Plasma amino acid patterns typical of PCS animals were observed: phenylalanine and tyrosine increased and branched chain AA decreased with shunting (p less than 0.05). Plasma phenylalanine increased further with 36P in PCS dogs (p less than 0.05), but was not affected by dietary protein concentration in controls. With 36P: CSF arginine, serine, histidine, tryptophan, phenylalanine, glutamate and glutamine increased in PCS dogs; but only arginine decreased in CSF of controls (p less than 0.05). In PCS dogs, significant CSF AA changes with elevated dietary protein were unrelated to plasma AA changes.

Eructation of gas through the gastroesophageal sphincter before and after limiting distension of the gastric cardia or infusion of a beta-adrenergic amine in dogs.

Gas eructation function of the gastroesophageal sphincter (GES) was investigated in 6 conscious dogs before and after a sleeve was placed around the GES and gastric cardia and during IV infusion of a beta-adrenergic amine (epinephrine). To induce eructation, nitrogen gas was insufflated (351.4 +/- 2 ml/min; mean +/- SEM) into the stomach through 1 channel of a 4-lumen catheter. After baseline studies and epinephrine infusion studies were completed in each dog, surgery was done to limit partially gastric distension by intraluminal contents by placing a silicone rubber sleeve around the GES and the first few centimeters of the cardia. Gastroesophageal sphincter pressure was 31.8 +/- 2.2 mm of Hg in baseline studies, 17.3 +/- 1.3 mm of Hg during epinephrine infusion (P. less than 0.003), and 30.3 +/- 2.2 mm of Hg after the sleeve was placed around the GES and cardia. During insufflation, gastric pressures before eructation increased to 5.74 +/- 0.41 mm of Hg before and to 15.15 +/- 1.63 mm of Hg after cardia sleeve placement (P less than 0.001). Eructation occurred at intervals of 1.83 +/- 0.41 minutes before cardia sleeve placement, and eructations were not observed with the sleeve in place. Before the sleeve was placed, administration of epinephrine resulted in an eructation interval of 0.84 +/- 0.09 minutes, which was significantly different from that in the same dogs given no drugs (P less than 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of corticosteroid treatment on survival time in dogs with chronic hepatitis: 151 cases (1977-1985)

Medical records of 151 dogs with chronic hepatitis were reviewed. Corticosteroid treatment had a statistically significant (P less than 0.005) effect on improving survival time when corticosteroid-treated dogs were compared with untreated dogs. Dogs dying within 1 week of examination represented 37.1% of the cases, and when compared with those living more than 1 week, serum glucose concentration was significantly lower (P less than 0.001); prothrombin time and partial thromboplastin time were significantly longer (P less than 0.001); blood ammonia concentration after oral administration of ammonium chloride was significantly higher (P less than 0.05); and necrosis severity and fibrosis severity were significantly greater (P less than 0.05 and P less than 0.022, respectively). The best predictors of early death were low normal serum glucose concentration (P less than 0.001) and prolonged prothrombin time (P less than 0.030), which was abnormal in 60.0% of dogs dying early. Partial thromboplastin time, which was increased in 92.0% of dogs dying early and in 42.6% of dogs living more than 1 week, was a less reliable predictor. Plasma ammonia concentration after oral administration of NH4Cl was least reliable in predicting early death. In dogs living more than 1 week, hypoalbuminemia was a predictor of shorter survival time (P less than 0.003). Of all the histologic features evaluated, only necrosis severity and fibrosis severity were accurate predictors of early death. The presence of bridging fibrosis was a predictor of shorter survival time in dogs living more than 1 week (P less than 0.0002).

Anal sphincter pressure and the rectosphincteric reflex in the dog.

Anal sphincter pressure (ASP) was measured in healthy conscious dogs, and the rectosphincteric reflex that causes inhibition of the internal sphincter was identified. Pressures were measured in 6 dogs by use of a perfused miniature 4-lumen catheter. To identify the rectosphincteric reflex, a balloon (fitted over the distal opening of the catheter) was insufflated with 25 ml of air. Mean (+/- SE) ASP was 74.7 +/- 4.2 mm of Hg. When the rectosphincteric reflex was stimulated by balloon distension, ASP decreased to 35.9 +/- 4.9 mm of Hg. The reduction in pressure persisted for 22 +/- 1.5 s, and ASP returned to predistension values, despite the maintenance of balloon distension. Atropine did not affect ASP or its reduction during balloon distension.

Eructation of gas through the gastroesophageal sphincter before and after gastric fundectomy in dogs.

The gas eructation function of the gastroesophageal sphincter (GES) was investigated in 6 conscious, fed dogs before and after gastric fundectomy. Using a perfused 4-lumen catheter with a Dent sleeve, gastric and GES pressures were measured. To induce eructation, nitrogen gas was insufflated (440 ml/min) into the stomach through one channel of the catheter. After base-line studies were completed on each dog, fundectomy, to remove 30% of the stomach, was performed. Mean (+/- SEM) GES pressure was 45.3 +/- 3.3 mm of Hg before fundectomy and 41.4 +/- 1.9 mm of Hg after fundectomy (P greater than 0.05). Before fundectomy, treatment with metoclopramide or cisapride increased GES pressure to 62.2 +/- 4.1 mm of Hg (P less than 0.001) and 61.1 +/- 5.0 mm of Hg (P less than 0.05), respectively. Gastric contraction rates were the same, 4.92 +/- 0.24/min and 4.80 +/- 0.16/min before and after fundectomy, respectively. During insufflation, gastric pressures before eructation increased to 12.2 +/- 1.3 mm of Hg before fundectomy and to 13.6 +/- 0.9 mm of Hg after fundectomy (P greater than 0.05). Eructation occurred at intervals of 1.44 +/- 0.20 minutes before fundectomy and 1.56 +/- 0.13 minutes after fundectomy (P greater than 0.05). Before fundectomy, administration of metoclopramide or cisapride resulted in eructation intervals of 1.72 +/- 0.21 minutes and 1.39 +/- 0.02 minutes, respectively; these intervals were not significantly different from those measured in dogs not given drugs. After fundectomy, the GES pressure in 5 dogs decreased and remained low during insufflation. After a series of normal eructation intervals, multiple eructations were observed in 4 of these dogs. Fundectomy did not impair ability to eructate gas from the stomach.

Eructation of gas through the gastroesophageal sphincter before and after truncal vagotomy in dogs.

The function of the gastroesophageal sphincter (GES) to eructate gas before and after vagotomy was investigated in conscious, fed dogs. Gastric and GES pressures were measured in 5 dogs, using a perfused 4-lumen catheter with a Dent sleeve. To induce eructation, nitrogen gas was insufflated (440 ml/min) into the stomach through 1 channel of the catheter. After base-line studies were completed on each dog, bilateral truncal vagotomy was performed 5 cm cranial to the diaphragm. Mean (+/- SE) GES pressure was 51.5 +/- 1 mm of Hg before vagotomy and 28 +/- 1.7 mm of Hg after vagotomy (P less than 0.001). Mean gastric contraction rates were the same, 4.91 +/- 0.11/min and 4.78 +/- 0.06/min in dogs before and after vagotomy, respectively. During insufflation, gastric pressures increased to 11.8 +/- 0.7 mm of Hg before eructation in dogs before vagotomy and to 18.4 +/- 0.8 mm of Hg in dogs after vagotomy (P less than 0.001). Eructation occurred at intervals of 1.79 +/- 0.09 minutes before vagotomy and 5.71 +/- 0.41 minutes after vagotomy (P less than 0.001). Atropine resulted in an interval of 1.98 +/- 0.18 minutes before vagotomy. Eructation was not seen in 2 dogs after vagotomy and was sometimes not seen in the 3 others. Gastroesophageal sphincter pressure in dogs before vagotomy began to decrease 4.5 +/- 0.2 s before the GES-pressure gradient disappeared, and GES pressure remained there for 5.3 +/- 0.3 s before the gradient began to return.(ABSTRACT TRUNCATED AT 250 WORDS)

Laboratory diagnosis of Giardia duodenalis infection in dogs.

Results of trichrome staining of fecal samples and intestinal contents preserved in polyvinyl alcohol fixative, fecal flotation utilizing unpreserved feces, and enzyme-linked immunosorbent assay of serum specimens were compared for the diagnosis of Giardia duodenalis infections in dogs. Trichrome staining of preserved fecal samples resulted in the identification of 44 (92%) of the 48 infected dogs from a group of 200 dogs. Trichrome staining of preserved intestinal contents resulted in the identification of 26 (54%) of the infected dogs, and fecal flotation resulted in the identification of 23 (48%) of the infected dogs. Giardia duodenalis antibodies were not detected consistently in the sera of infected dogs.

Use of pulmonary hydrogen gas excretion to detect carbohydrate malabsorption in dogs.

Pulmonary H2 excretion was measured in 10 healthy dogs, in 6 dogs with pancreatic exocrine insufficiency, and in 6 dogs with chronic small intestinal disease. Concentration of expired H2 in fasted healthy dogs was 0.9 +/- 0.1 ppm (mean +/- SEM) and peak H2 concentration of 1.4 +/- 0.2 ppm was detected up to 8 hours after feeding. Dogs with pancreatic exocrine insufficiency had fasting expired H2 concentrations of 3.3 +/- 0.9 ppm, which increased to a mean peak H2 concentration of 28.8 +/- 2.0 ppm 6.5 hours after feeding. Following xylose administration, expired H2 concentrations increased from fasting concentrations of 3.6 +/- 0.9 ppm to peak at 19.0 +/- 2.0 ppm in 1.5 hours. Blood xylose concentrations were diagnostic for carbohydrate malabsorption in 4 of 6 dogs with pancreatic exocrine insufficiency. Plasma p-aminobenzoic acid concentration identified bentiromide maldigestion in all dogs with pancreatic exocrine insufficiency. In 3 pancreatic exocrine insufficient dogs tested, pancreatic enzyme replacement therapy partially corrected carbohydrate malabsorption. Fasting expired H2 concentration was 5.3 +/- 1.3 ppm in dogs with chronic small intestinal disease and increased to a peak H2 of 72.2 +/- 18.0 ppm 7 hours after feeding. Following administration of xylose to dogs with chronic small intestinal disease, fasting expired H2 concentration increased from 3.0 +/- 1.0 ppm to a peak of 35.5 +/- 7.2 ppm at 2 hours. Blood xylose concentration was abnormal in only 2 of 6 dogs with chronic small intestinal disease. Results of these studies indicate that expired H2 analysis can identify carbohydrate malabsorption in dogs with pancreatic exocrine insufficiency or chronic small intestinal disease, and that pulmonary H2 testing is more sensitive than xylose absorption testing for the identification of carbohydrate malabsorption.

Evaluation of intestinal carbohydrate malabsorption in the dog by pulmonary hydrogen gas excretion.

Breath H2 was measured for the assessment of intestinal carbohydrate absorption in healthy, fasted dogs before and after the ingestion of carbohydrate test meals. The dogs were fed lactulose, xylose, glucose, a hypoallergenic diet, or the hypoallergenic diet supplemented with rice, corn, or wheat flour. Breath samples for H2 analysis were collected by an interval-sampling technique during tidal breathing and were analyzed by thermal conductivity gas chromatography. Pulmonary H2 excretion in fasted dogs never exceeded 1 part per million (molecules of H2 per 10(6) molecules of air). Breath H2 excretion after the ingestion of 12.5 g of glucose, a completely absorbed monosaccharide, was not significantly different (P greater than 0.05) from that during fasting; however, ingestion of 12.5 g of xylose, an incompletely absorbed pentose, significantly increased (P less than 0.001) breath H2 excretion. After ingestion of 12.5, 25, or 50 g of lactulose, a nonabsorbable disaccharide, pulmonary H2 excretion increased significantly (P less than 0.001) over fasting amounts and the increases were different (P less than 0.001) from one another. Increases in breath H2 excretion correlated (r = 0.97) with increases in lactulose dose. Breath H2 excretion after the ingestion of the hypoallergenic diet did not significantly (P greater than 0.05) differ from that after fasting. The addition of rice flour to this diet did not significantly (P greater than 0.05) increase H2 production. However, the addition of wheat or corn flour to this diet significantly (P less than 0.001) increased breath H2 excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical and pathologic changes in experimentally induced acute pancreatitis in cats.

Acute pancreatitis was induced in 6 cats by infusion of oleic acid into the pancreatic duct. Clinical changes included fever, tachycardia, and variable degrees of abdominal pain; vomiting occurred rarely, and diarrhea was not noted. Serum lipase activities were significantly increased through the 4th day after the surgical operation, although amylase activities were significantly decreased during most of the acute phase. Serum calcium and phosphate concentrations were decreased significantly on the 4th day after surgical operation. Hematologic alterations included normocytic, normochromic, responsive anemias, but changes in WBC values were not statistically significant. Evidence of exocrine pancreatic insufficiency after induction of acute pancreatitis was not demonstrated in any cats during the study. The results of this study indicate that increases in serum lipase activity are the most consistent and earliest indicators of acute pancreatitis in cats, but that more sensitive methods of laboratory evaluation should be sought.

Long-term biochemical and physiologic effects of surgically placed portacaval shunts in dogs.

After surgical placement of end-to-side portacaval shunts (PCS), 4 adult mongrel dogs (11.8 to 18.2 kg) were fed purified diets and monitored for approximately 50 weeks for changes in body weight, neurologic status, and an array of clinically important biochemical variables. Two healthy dogs, fed the same diets and maintained in the same environment, were also observed (controls). Body weights were relatively stable over the period of observation. The branched-chain ratio ([valine] + [leucine] + [isoleucine]/[phenylalanine] + [tyrosine]), an index of the degree of change in plasma amino acid concentrations, was significantly lower in dogs with PCS than in controls. Despite this depression in branched-chain ratio, the principals (dogs with PCS) were essentially free of neurologic symptoms. Statistically significant decreases due to portacaval shunting were seen in the serum concentrations of glucose, calcium, urea nitrogen, creatinine, cholesterol, and albumin. Total protein, globulin, and triglyceride concentrations tended to be lower in the serum of principals than in serum of controls, but the differences were not statistically significant. Statistically significant increases due to portacaval shunting were seen in plasma concentrations of total conjugated bile acids and sulfobromophthalein retention. Concentrations of the following compounds tended to be higher in serum of principals than in serum of controls: phosphorus, chloride, uric acid, total bilirubin, lactate dehydrogenase, aspartate transaminase, alanine transaminase, and alkaline phosphatase. Liver biopsy at 7 months after operation showed mild-to-extensive atrophy of hepatocytes, mild-to-extensive fibrosis, and collapsed portal veins in all principals examined.

Application of the log-linear model in the prediction of the antinuclear antibody test in the dog.

To find possible associations between antinuclear antibody (ANA) pattern, ANA titer, and certain clinical changes and clinical laboratory test results in dogs, the veterinary medical records of 111 ANA-positive and 126 ANA-negative dogs were examined. Variables could not be found that had significant associations with ANA pattern (unlike the results in persons), because of the predominance of 2 patterns. A log-linear model for ANA titer adequately fit the observed frequency and included 2-way interactions between titer and polyarthritis, titer and hematologic disorders, and polyarthritis and lymphadenopathy.

Application of the log-linear and logistic regression models in the prediction of systemic lupus erythematosus in the dog.

This study sought to mathematically define canine systemic lupus erythematosus (SLE) by unifying diagnostic criteria proposed by others. Thirty-one cases of canine SLE were selected for modeling when 4 different published schemes agreed on the diagnosis, and 122 controls were selected when a patient's status met no scheme's criteria. The log-linear method showed an association between SLE and polyarthritis, hematologic abnormalities, renal damage, dermatologic disorders, and antinuclear antibody test response (positive). Logistic regression was then used to derive a predictive algorithm that could identify cases and controls with which all published criteria would be in accordance. The final equation correctly classified 93.5% of the affected dogs and 98.4% of the controls. It was concluded that the log-linear and logistic regression models are useful for the diagnosis of clinically similar, but distinguishable, disease states.

Effect of gastrin, histamine, serotonin, and adrenergic amines on gastroesophageal sphincter pressure in the dog.

In nonrestrained dogs that had not been given chemicals and that were in the fasted and fed state, gastroesophageal sphincter pressure (GESP) was measured; results were compared with GESP induced in the same dogs by drugs that modified activity at cholinergic, adrenergic, histaminic, and gastrin receptors. Atropine reduced GESP from 38.5 +/- 1.3 (mean +/- SE) and 55.5 +/- 2.0 mm of Hg to 11.3 +/- 2.0 and 14.5 +/- 2.4 mm of Hg in fasted and fed dogs, respectively. Histamine induced phasic contractions that were not affected by anticholinergics or cimetidine. Iphenhydramine eliminated the phasic contractions and reduced GESP to 18.2 +/- 3.9 mm of Hg. In fed dogs, diphenhydramine reduced GESP to 37.0 +/- 2.5 mm of Hg, but cimetidine did not. Pentagastrin induced increases in GESP that were inversely related to basal GESP. Pentagastrin given during histamine infusion eliminated histamine-induced phasic contractions. In fed dogs, metoclopramide increased GESP from 48.8 +/- 4.0 mm of Hg to 76.0 +/- 4.0 mm of Hg; this increment was eliminated by diphenhydramine. Administration of atropine after metoclopramide reduced GESP the same as for dogs given atropine alone. An adrenergic amine with only alpha-adrenergic effects induced phasic contractions, and an adrenergic amine with only beta-adrenergic effects reduced GESP. Blockers of alpha and beta effects did not change GESP in fed dogs. Domperidone induced phasic contractions that were eliminated by feeding. Serotonin increased GESP. Canine GESP may be maintained in fed dogs by chemicals interacting with cholinergic, histaminic, gastrin, and serotonin receptors, but not by chemicals interacting with adrenergic receptors.

Effects of atropine, acepromazine, meperidine, and xylazine on gastroesophageal sphincter pressure in the dog.

Gastroesophageal sphincter (GES) pressure was 47.9 +/- 1.2 mm of Hg in nontreated dogs. Treatment with atropine, acepromazine, and xylazine reduced GES pressure to 13.2 +/- 2.03, 18.6 +/- 2.14, and 11.7 +/- 1.19 mm of Hg, respectively. Treatment with meperidine resulted in phasic contractions with minimum and maximum pressures of 27.9 +/- 4.55 and 98.9 +/- 9.16 mm of Hg, respectively. Drugs used in anesthetic procedures can reduce GES pressure in dogs.

Effects of catecholamines and ammonia on plasma and brain amino acids in dogs.

Investigations were made on the effects of catecholamine (Cat) infusions with and without ammonia (NH3) on plasma and brain amino acids (AA) and brain neurotransmitters in dogs. Groups of four dogs were infused for 5 h with epinephrine (E), epinephrine + norepinephrine (E + NE), epinephrine + norepinephrine with NH3 during h 4 and 5 (E + NE + NH3), epinephrine + norepinephrine + tryptophan with NH3 during h 4 and 5 (T + E + NE + NH3), or saline (C). Cat decreased (P less than 0.05) plasma Gly, Thr, Lys, Pro, Val, Ser, Arg, Leu, Trp, Phe, Asn, Tyr, Met, Ile, Cit, and Asp. The decreases at h 3 for all were to a mean of 45% of 0 h and were associated with no changes in plasma insulin or glucagon. Cat increased plasma Tau and Orn. Of the most abundant brain AA (82% of total), E + NE + NH3 had no effect (GABA, Asp, Gly, Ala, p-ethanolamine) or increased (Glu, Gln, Tau) brain levels. These AA were unchanged by Cat alone. Of the remaining brain AA, most were decreased by Cat (7 of 16, P less than 0.05) and E + NE + NH3 increased brain Trp but had no effect on brain serotonin, 5-hydroxyindoleacetic acid, or NE. Cat changed plasma AA in a way similar to changes produced by NH3 infusion and seen with hepatic insufficiency due to portacaval shunts and nitrosamine-induced pathology. Cat reduced brain AA levels, and this was partially restored by NH3.