Ureterocolonic anastomosis was evaluated in 13 clinically normal dogs. Urinary continence was maintained after surgery, and the procedure was completed without technique errors in all but 2 dogs. Three dogs died within 5 weeks (2 of undetermined causes and 1 of aspiration pneumonia and neurologic disease), and 1 dog was euthanatized 4 months after surgery because of neurologic signs. Two healthy dogs were euthanatized 3 months after surgery for light microscopic evaluation of their kidneys. Five dogs were euthanatized 6 months after surgery for light microscopic evaluation of their kidneys. Gastrointestinal and neurologic disturbances developed in 4 dogs at various postoperative intervals. Plasma ammonia concentration measured in 2 dogs with neurologic signs was increased. Plasma ammonia concentration measured in 5 dogs without neurologic signs was within normal limits. All 5 dogs, in which metabolic acidosis was diagnosed, had high normal or above normal serum chloride concentration. Serum urea nitrogen values were increased after surgery because of colonic absorption of urea. Serum creatinine concentration was increased in 1 dog 6 months after surgery. Individual kidney glomerular filtration rate was reduced in 38% (3/8) of the kidneys from 4 other dogs at 6 months after surgery. Of 5 dogs euthanatized at 3 to 4 months after surgery, 4 had bilateral pyelitis, and 1 had unilateral pyelonephritis. Six months after surgery, pyelonephritis was diagnosed in 40% (4/10) of the kidneys from 5 dogs. The ureterocolonic anastomosis procedure is a salvage procedure that should allow complete cystectomy. However, variable degress of metabolic acidosis, hyperammonemia, and neurologic disease may result.

In this study, immunohistochemistry was used to examine the changes in the density of colonic endocrine cells - argyrophil and argentaffin cells, chromogranin A (CGA), serotonin, somatostatin and glucagon-containing cells in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis. Ulcerative colitis was induced by the instillation of 10 mg of TNBS into the colonic lumen through the anus. To confirm the inducement of ulcerative colitis, the macroscopic and microscopic scores as well as the colonic myeloperoxidase (MPO) activities were monitored for 8 days after TNBS instillation in the colonic lumens. In addition, the number of argyrophil and argentaffin cells, CGA, serotonin, somatostatin and glucagon-immunoreactive cells were counted in the colonic mucosa, respectively. After TNBS instillation into the lumen of the colon from the anus in rats, increases in macroscopic and microscopic scores in the colon tissues were observed along with increases in the colonic MPO activities. Therefore, ulcerative colitis was relatively well induced by the TNBS instillations. Marked decreases in the number of colonic endocrine cells were detected in the TNBS-treated animal compared to the sham control. These results suggest that colonic endocrine cells were also disrupted by TNBS-induced ulcerative colitis.

The cases of feline panleukopenia virus (FPLV) infection were diagnosed in three imported cats. All cats died within one week after mild emaciation, depression and anorexia. One cat showed yellowish watery diarrhea. At necropsy, all cats had segmental hemorrhage on the serosa and mucosa of the small intestine. Histopathologically, severe diffuse necro-hemorrhagic enteritis was observed in small intestine especially in jejunum and ileum. The crypts of Lieberkuhn were dilated and contained necrotic epithelia. Severely damaged epithelia of crypts were transformed into bizarre shapes.

Diaphragmatic hernias, whether congenital or acquired (traumatic), are rarely observed in the horse. Acquired diaphragmatic hernias typically occur secondary to trauma or an increase in intra-abdominal pressure due to falling, heavy exercise, or parturition. Diaphragmatic herniorrhaphy is difficult to perform in adult horses and the horses with symptomatic diaphragmatic hernias usually die. A 10-year old, 340 kg, Jeju horse (crossbred) broodmare with sudden onset of gait disorder and a moderate emaciation was examined. Findings on physical examination included conjunctivitis, dehydration, shallow breathing, dyspnea, weaken heart beat, lack of auscultatable sounds from the gastrointestinal tract, and anorexia. Rectal temperature was 38.4℃ and respiratory rates were moderately increased. There were slight signs of acute colic. The broodmare died one day after non-specific treatment of fluids, nutriment, antibiotics and non-steroidal anti-inflammatory drug. The cause of death was strangulation of the small intestine through a diaphragmatic hernia. The rent was about 2 cm in diameter and located in the central right part of diaphragm. Around 60 cm of small intestine was protruded into thoracic cavity through the rent. The cause of the hernia could not be ascertained. The broodmare had been pastured with many other horses, and the groom had not noticed any aggressive behavior among them. It was, however, speculated that trauma by stallion's attack may have been the cause of the diaphragmatic hernia, because the new horse may be the object of behaviors ranging from mild threats to seriously aggressive kicking, squealing, rearing, and biting.

The purpose of this study was to evaluate the relationship between the results of laboratory examinations and ultrasonographic findings, especially portal vein hemodynamics in experimentally bile duct ligated dogs. Biliary obstruction was accomplished by surgically occluding the common bile duct in five dogs. All the dogs became visibly jaundiced within 24 hours after surgery. The total protein and albumin/globulin ratio showed a gradual decrease throughout the examination period, while blood urea nitrogen reached its peak in the 6th week and decreased to pre ligation values by the 10th week. Similar trends were noted in the alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and direct and total bilirubin. Total cholesterol and fasting serum bile acid levels rapidly increased after surgery to peak values between the 2nd and 4th week, and then gradually decreased, but still remained high throughout the experiment period. The portal flow volume and velocity significantly (p0.05) decreased while only a slight increase was noted in the congestion index after bile duct ligation. The cross sectional area of the portal vein changed insignificantly. Bile duct and gallbladder distention was evident within the 1st week after ligation but there was little change in the echogenicity of the liver parenchyma. The results of this study suggest that the determination of Doppler ultrasound parameters of hepatic hemodynamics, especially the portal vein flow indices, may contribute to a better noninvasive assessment of the canine patient with biliary obstructive disease