The initial soil microbiota impacts the potential for lignocellulose degradation during soil solarization.

AIMS: Soil biosolarization (SBS) is a pest control technology that includes the incorporation of organic matter into soil prior to solarization. The objective of this study was to measure the impact of the initial soil microbiome on the temporal evolution of genes encoding lignocellulose-degrading enzymes during SBS. METHODS AND RESULTS: Soil biosolarization field experiments were completed using green waste (GW) as a soil amendment and in the presence and absence of compost activating inoculum. Samples were collected over time and at two different soil depths for measurement of the microbial community and the predicted lignocellulosic-degrading microbiome. Compost inoculum had a significant positive effect on several predicted genes encoding enzymes involved in cellulose, hemicellulose and lignin degradation. These included beta-glucosidase, endo-1,3(4)-beta-glucanase, alpha-galactosidase and laccase. CONCLUSION: Amendment of micro-organisms found in compost to soil prior to SBS enhanced the degradation potential of cellulose, hemicellulose and lignin found in GW. SIGNIFICANCE AND IMPACT OF THE STUDY: The type of organic matter amended and its biotransformation by soil micro-organisms impact the efficacy of SBS. The results suggest that co-amending highly recalcitrant biomass with micro-organisms found in compost improves biomass conversion during SBS.

Pharmacokinetics of allopurinol in Dalmatian dogs.

The pharmacokinetics of allopurinol were studied in Dalmatian dogs. Eight dogs were given allopurinol orally at a dose of 10 mg/kg for seven doses prior to sample collection. After a period of at least two weeks, four of these dogs and four additional Dalmatians were later given a single intravenous (i.v.) dose of allopurinol (6 mg/kg) prior to sample collection. Allopurinol was found to follow first-order absorption and elimination kinetics. In the i.v. kinetic study, the elimination constant (Kel) = 0.31 +/- 0.03 per h, the half-life (t1/2) = 2.22 +/- 0.20 h, the initial concentration (C0) = 5.26 +/- 0.34 micrograms/mL and the specific volume (Vd) = 1.14 +/- 0.07 L/kg. Clearance of allopurinol was estimated to be 0.36 +/- 0.03 L/kg.h. In the oral kinetic study, the absorption rate constant (Kab) = 1.06 +/- 0.13 per h, the elimination rate constant (Kel) = 0.26 +/- 0.01 per h, the absorption half-life (t1/2ab) = 0.66 +/- 0.06 h, and the elimination half-life (t1/2el) = 2.69 +/- 0.14 h. Peak plasma concentrations (Cmax) = 6.43 +/- 0.18 micrograms/mL were obtained within 1 to 3 h (mean time of maximum concentration (Tmax) = 1.9 +/- 0.1 h). The volume of distribution corrected by the fraction of dose absorbed (Vd/F) was estimated to be 1.17 +/- 0.07 L/kg. Good agreement was obtained between mean kinetic parameters in the oral and i.v. studies. There was little variation between individual dogs in the i.v. study, whereas the rate of absorption and elimination of orally administered allopurinol was more varied among individual dogs. Because of this, and the fact that the magnitude of hyperuricosuria varies among Dalmatians, it is not possible to specify an exact dose of allopurinol that will effectively lower the urinary uric acid concentration to acceptable values in all Dalmatians with hyperuricosuria; rather, the dose must be titrated to the needs of each dog.

[3H]ouabain binding in skeletal muscle from horses with hyperkalemic periodic paralysis.

Ouabain, a cardiac glycoside, binds to the Na(+)-K(+)-adenosine triphosphatase (Na+ pump) and prevents active transport of Na+ and K+ across cell membranes. We used [3H]ouabain to quantify the number and affinity of Na+ pumps in skeletal muscle from Quarter Horses with the muscular disorder hyperkalemic periodic paralysis (HYPP). [3H]Ouabain-binding properties of gluteal muscle from clinically normal and affected horses were used to determine whether altered Na+ pump number or affinity could contribute to the pathologic features of muscle in affected horses. Foals and adult horses with HYPP were compared with age-matched clinically normal horses. The number of [3H]ouabain-binding sites in adult gluteal muscle was not different between the 2 types of horses (85.7 +/- 8.9 pmol of [3H]ouabain-binding sites/g [wet muscle weight] in horses with HYPP vs 100.2 +/- 8.8 pmol/g in clinically normal adult horses). Gluteal muscles in HYPP-affected and clinically normal foals also contained a similar number of [3H]ouabain-binding sites (222.3 +/- 21.0 pmol/g vs 225.3 +/- 24.2 pmol/g, respectively). The affinity of these binding sites for ouabain was not different, between adults or foals, in clinically normal or affected horses. Our results indicate that membrane events underlying the periodic episodes of paralysis in horses with HYPP are not attributable to quantitative changes in Na+ pump number or affinity. Our data cannot exclude the possibility that the specific activity of the Na+ pump is altered in muscle from HYPP-affected horses.

Genetic study of hyperkalemic periodic paralysis in horses.

Four Quarter Horses (1 stallion, 3 mares) with hyperkalemic periodic paralysis were mated to unaffected horses to determine the genetic basis of the disease. The affected stallion was bred to 11 unaffected mares (4 Quarter Horses, 1 Arabian, 2 Standardbreds, and 4 Thoroughbreds). The 3 affected mares were bred to an unaffected Quarter Horse stallion. Of the 15 offspring obtained from these matings, 9 were affected with hyperkalemic periodic paralysis, and 6 were unaffected, consistent with an autosomal dominant mode of inheritance. Diagnosis was established by results of oral administration of potassium chloride and demonstration of characteristic clinical signs accompanied by hyperkalemia. Oral administration of potassium chloride resulted in marked increases in plasma potassium concentrations in affected and unaffected foals, although hyperkalemia was associated with clinical signs of hyperkalemic periodic paralysis in the affected foals. Evaluation of blood samples from affected and unaffected offspring revealed no linkage with erythrocyte and serum markers at 24 loci.

Xanthine-containing urinary calculi in dogs given allopurinol.

Clinical features and laboratory findings were evaluated in 10 dogs that formed xanthine-containing urinary calculi during the period that they were given allopurinol (9 to 38 mg/kg of body weight/d). Duration of allopurinol treatment was 5 weeks to 6 years. Of the 10 dogs, 9 (all Dalmatians) had formed uric acid-containing calculi at least once before allopurinol treatment was initiated. It was not possible to recognize xanthine as a crystalline component of the calculi by use of a chemical colorimetric method or by polarized light microscopy. We concluded that the best diagnostic method for recognition of xanthine-containing calculi was high-pressure liquid chromatography because it is quantitative, sensitive, and accurate, and can be conducted on a small amount (1 to 2 mg) of crystalline material.

Furosemide and sodium bicarbonate-induced alkalosis in the horse and response to oral KCl or NaCl therapy.

Metabolic alkalosis was induced in 10 clinically normal horses by administration of furosemide (1 mg/kg of body weight, IM) followed 4.5 hours later by sodium bicarbonate (NaHCO3; 500 g in 8 L water) via nasogastric tube. Furosemide diuresis resulted in a mean weight loss of 21.1 kg, which was associated with small, but significant, increases in venous blood pH, bicarbonate, and plasma protein concentrations (P less than 0.001), while plasma potassium, chloride, and calcium concentrations declined significantly (P less than 0.001). Oral administration of the hypertonic NaHCO3 solution resulted in clinical evidence of hypovolemia, which was accompanied by a marked increase (P less than 0.001) in plasma protein concentration. Seven of the 10 horses developed signs of neuromuscular excitability, as evidenced by muscle fasciculations, and 5 of the horses developed diaphragmatic flutter. Hypernatremia was transiently induced, but it resolved as the horses were allowed access to water. The alkalosis induced by furosemide and NaHCO3 was profound and persisted for a 24-hour period and was associated with marked hypochloremia and hypokalemia. Partial replacement of the electrolyte deficits and correction of the metabolic alkalosis was attempted, using 1,000 mEq of NaCl or KCl given as an isotonic solution via nasogastric tube. In the KCl-treated group, there was a prompt and significant decline in venous blood pH and bicarbonate concentration (P less than 0.001) accompanied by a significant increase in plasma potassium concentration (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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).

Influence of furosemide treatment on fluid and electrolyte balance in horses.

Alterations in electrolyte and acid-base balance were studied in 6 horses for 8 hours after furosemide administration (1 mg/kg of body weight, IM), and the results were compared with those for 5 healthy untreated horses (controls) kept under identical environmental conditions. In the treated group, decreases in plasma potassium, chloride, and calcium concentrations and increases in total plasma protein content persisted for the 8-hour observation period, whereas there was no change in plasma sodium concentration, osmolality, or packed cell volume. Plasma bicarbonate concentration and PCO2 remained high throughout the study, during which time venous blood pH was modestly increased only at the 6-hour sampling time. Furosemide treatment resulted in decreases in urine pH, specific gravity, osmolality, and potassium and calcium concentrations and increases in urine volume and total urine sodium, chloride, and calcium excretion. Body weight decreased 19.2 +/- 5.2 kg (mean +/- SD) in treated horses (4 +/- 1% of body weight), compared with a weight loss of 8 +/- 2.1 kg in untreated horses (1.5 +/- 0.4% of body weight) during the 8-hour experimental period. The increased fluid losses induced by the diuretic did not cause any obvious clinical signs in the horses. Pulse pressure, skin turgor, capillary refill time, and jugular distensibility remained unchanged throughout the experimental period.

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.

Plasma, red blood cell, total blood, and extracellular fluid volumes in healthy horse foals during growth.

During the growth interval encompassing age 2 days through 24 weeks, plasma, RBC, total blood, and extracellular fluid (ECF) volumes were determined in 7 healthy, resting foals. Evans blue dye and sodium thiocyanate were used to estimate plasma and ECF volumes, respectively. Absolute plasma volume remained stable from 2 days through 2 weeks of age, then increased progressively through 24 weeks of age. After decreasing between 2 days and 2 weeks of age, absolute RBC and total blood volumes progressively increased. Absolute ECF volume increased progressively from 2 days of age through 24 weeks of age, but plasma, RBC, and total blood volumes decreased relative to body weight increase. During the first 12 weeks of life, ECF volume decreased relative to body weight increase, and then remained stable during the next 12 weeks. There were close correlations between age, as well as body weight, and plasma, RBC, total blood, and ECF volumes. The relationship defined between age and the respective fluid and blood volumes provided a useful tool for evaluation and management of alterations of fluid balance in the foal.

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)

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.

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.

Model of chronic pancreatitis in the dog.

A model of chronic pancreatitis was developed and characterized in the dog. Pancreatitis was produced by infusion of oleic acid through a cannula in the accessory pancreatic duct. Biochemical changes included early and marked increases in serum amylase and lipase activities which returned to base line within 3 weeks, at which time the dogs were clinically normal. In dogs euthanatized within 2 weeks, pathologic changes included massive necrosis and hemorrhage, cystic spaces filled with fluid, and abscesses. Histologic features revealed acute exudative pancreatitis with pancreatic atrophy and fibrosis. In dogs killed between weeks 3 to 12, changes included: marked atrophy with remaining acini surrounded by remnants consisting of collapsed stroma, blood vessels, and pancreatic ducts; marked coarse fibrosis with scattered inflammatory cells and occasional acinar tissue; and large irregular pseudocysts.