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The pathology of malignant hypertension in dogs induced either purposely or inadvertently by the Goldblatt procedure has not been previously reported. Malignant hypertension was experimentally produced in beagle dogs by a modified Goldblatt procedure; in a single surgical procedure, one kidney was removed and the blood flow to the remaining kidney was reduced by 50%. A sudden onset of severe clinical signs developed within one to three weeks after surgery. The dogs were markedly depressed or in shock, were vomiting, and had either bloody feces or bloody diarrhea. Hematologic changes compatible with a diagnosis of microangiopathic hemolytic anemia consisted of hemolysis, thrombocytopenia, and the presence of burr cells and schistocytes. Some dogs had neutrophilia and slight to moderate increases in blood urea nitrogen and creatinine. At necropsy, there were gross hemorrhages in the heart, brain, urinary bladder, and gastrointestinal tract. Histologic findings consisted of multifocal parenchymal hemorrhage, fibrinoid necrosis of arterioles, medial smooth muscle hyperplasia, adventitial fibroplasia and mononuclear cell infiltrates, and microthrombi. The vascular clamp most likely protected the kidney from the systemic hypertension since the remaining kidney was largely not remarkable by light or electron microscopy. The dog appears to be a good model to study the pathology of malignant hypertension and microangiopathic hemolytic anemia.

Strangulation obstruction was induced in anesthetized ponies for periods of 2 and 3 hours by clamping 45-cm segments of jejunum and their veins only (venous strangulation obstruction, VSO) and arteries and veins (arterial and venous strangulation obstruction, AVSO). These types of strangulation obstruction were studied in 4 segments in each of 4 ponies allowed to survive 12 hours (group 1) and in a single segment in each of 10 ponies allowed to survive 42 days (group 2) after the strangulation period ended. On visual inspection, segments subjected to VSO had hemorrhage and edema in the bowel wall and mesentery and were dark purple after all time intervals. They improved slowly after clamps were removed, but remained hemorrhagic and edematous. Segments subjected to AVSO were purple and had mild edema and scattered petechiae in the bowel wall and mesentery. They improved rapidly and closely resembled normal bowel after 5 minutes of reperfusion. On light and scanning electron microscopy, the mucosa of intestine subjected to VSO and AVSO had necrotic, denuded villi 1 hour after the strangulation periods ended. Twelve hours after removal of occlusion devices in group-1 ponies, 4 (25%) segments were unchanged, 4 (25%) had deteriorated, and 8 (50%) had stunted villus remnants partly or completely lined with regenerating epithelium. Separation and detachment of villus tip mucosal cells were seen in 3 of 4 control segments, 1 and 12 hours after the strangulation periods ended.(ABSTRACT TRUNCATED AT 250 WORDS)

Corynebacterium equi is a pathogen associated with respiratory disease in the foal. This paper discusses two cases of Corynebacterium equi infection, one acute and one chronic, in which the major damage was intestinal. Necrosis of Peyer's patches was the only lesion seen in the small intestine of both foals. The foal with acute disease had distinct green-tan focal necrosis and thickened mucosa of the large intestine. In the foal with chronic disease, the mucosa of the large intestine was thickened, rugose, and mottled red-tan. Histologically, the predominant lesions were villous atrophy, mucosal necrosis, mesenteric lymph node necrosis and large numbers of periodic acid Schiff (PAS)-positive macrophages filled with gram-positive pleomorphic bacilli. Electron microscopy of intestinal mucosa showed bacilli undergoing binary fission in macrophages and bacilli free in the lamina propria.

The D-xylose absorption test was applied to clinically normal horses and to horses with signs of gastrointestinal disease. A dosage of 0.5 grams of xylose per kilogram of bodyweight was useful in detecting horses that absorbed the pentose abnormally. The clinical findings were correlated with gross and microscopic findings by biopsy and at necropsy. Gastrointestinal lesions associated with abnormal xylose absorption were classified as: 1) villous atrophy; 2) edema of the lamina propria or 3) necrosis of the lamina propria.

Granulomatous enteritis was diagnosed in 9 horses between 1 and 11 years of age. The complaint in all cases was persistent weight loss. Four of the horses had chronic diarrhea. Two consistent diagnostic features were hypoalbuminemia and decreased phagocytic activity of mesothelial cells in the peritoneal fluid. In 2 cases the diagnosis was confirmed by biopsy of the rectal mucosa. Remaining cases were definitively diagnosed by exploratory laparotomy and biopsy or at necropsy.

Five clinically normal, mature horses and 11 with chronic diarrhea were given 51Cr-tagged Cohn fraction V equine albumin intravenously. All urine and feces were collected separately, and blood for plasma analysis was taken periodically for 5 to 8 days after injection of the isotope. Plasma clearance of albumin into the intestinal tract of normal horses was calculated as 0.67 +/- 0.23 (SD) ml/kg of body weight/day, with 1.33 +/- 0.69% of the 51Cr dose appearing in the feces in 5 days. Of the 11 diarrheal horses, 8 had a plasma clearance of 0.49 +/- 0.21 ml/kg/day with 1.12 +/- 0.68% of the dose of 51Cr in a 5-day fecal collection, suggesting that excessive losses of plasma protein into the bowel was not a component of their intestinal disease. The 3 other diarrheal horses had a marked protein-losing enteropathy; 1 of these horses had granulomatous enteritis due to Mycobacterium avium infection; another had severe intercellular edema of small and large intestinal mucosa, cause unknown; and intestinal biopsies were not obtained from the 3rd horse. The results suggest that: (1) as with other species that have been studied, daily loss of plasma protein into the bowel of horses is small; (2) most horses with chronic diarrhea do not have protein-losing enteropathy.

We evaluated the effects of maternal administration of vitamin A acetate on pup development and behavior. Vitamin A acetate was administered by oral gavage to pregnant rats (N = 10/treatment) on gestation days 6-19 at doses of 25,000, 50,000 or 100,000 I.U./kg/day. Male and female pups from dams that received 100,000 I.U./kg/day showed a significantly reduced live birth index but few external abnormalities. Twenty-four and 48 hour survival indices were also significantly reduced. The mean pup body weight gain at 100,000 I.U./kg/day was significantly reduced at days 1-3, 3-7 and 21-42. Pinna detachment and eye opening were significantly delayed in all male pups and in female pups from the 50,000 and 100,000 I.U./kg/day groups. Incisor eruption was significantly delayed in male and female pups from the 25,000 and 50,000 I.U./kg/day groups. The following showed no treatment effects: dam mean weight change, length of gestation, total litter size, surface righting, cliff avoidance, negative geotaxis, swimming development, open field activity and discriminatory learning.

The gross and histopathologic findings seen in the stomach of rats treated with an H2-antagonist, tiotidine, will be presented. The data presented is from two studies, a six month oral (gavage) and dietary study in male rats, and a 12 month oral chronic toxicity study combined with a 24 month oncogenicity feeding study in rats. Significant findings in the stomach included fundic glandular dilatation, parietal cell atrophy, metaplastic fundic cells, fundic nuclear clusters, and dysplasia/carcinoma lesions. The chronology of the borderline type dysplasia/carcinoma lesions starting from the very early to the more advanced infiltrating carcinomas will be shown. A total of 17 rats with lesions of the dysplasia/carcinoma complex out of 828 treated rats from the two studies were present. No similar type lesions were seen in any of the 432 control rats examined. The importance of the diagnostic methods used in the examination of the stomach is stressed.

Repeated direct puncture of the central ear (intermediate auricular) artery to obtain mean arterial blood pressure in control and hypertensive dogs was evaluated. Unilateral nephrectomy and partial constriction of the contralateral renal artery were performed on four dogs to create hypertension. Ear artery blood pressure measurements and electrocardiograms were recorded twice pretest and after surgery at Weeks 1, 2, 4, 6, 8, 9, 10, and 11 on control (n = 6) and hypertensive (n = 4) dogs. Mean ear arterial blood pressures from the hypertensive dogs were significantly increased from Weeks 2 to 11. Indwelling omocervical artery catheters were implanted in both control and hypertensive dogs at Week 8. Mean omocervical artery blood pressures from hypertensive dogs were significantly increased at Weeks 8 through 11. Mean omocervical artery pressures were only significantly increased over mean ear artery pressures at Week 8 for control dogs and at Week 10 for hypertensive dogs. Nonspecific electrocardiographic changes in the ST-T segment and U waves occurred with greater frequency in hypertensive dogs than in control dogs. Hypertensive dogs developed subendothelial proliferation in the renal artery and aorta, and a proliferative vasculopathy in the heart and lungs. This ear artery technique was used successfully in two canine toxicity studies of different ICI pharmaceutical compounds. The ear artery method for measuring mean arterial blood pressure is suitable for canine toxicity studies and is a reasonably accurate measurement of systemic pressure.