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Multicompartmental analysis was applied to study the kinetics of D-xylose distribution after its intragastric administration to healthy mares deprived of food for 12, 36, 72, and 96 hours. Disposition of D-xylose was described by a 5-compartment model. Maximal plasma D-xylose concentration was similar for 12 and 36 hours of food deprivation and was greater (P = 0.0001) than the values for 72 and 96 hours. Peak concentration of D-xylose appeared progressively later as food deprivation proceeded (P = 0.0001). Fractional rate of transfer (k1,6) was less after 96 hours of food deprivation, compared with 12 hours (P = 0.0001), and percentage of D-xylose absorbed was reduced (P = 0.0441) after food deprivation. Fractional rate of transfer (k6,5), representing gastric emptying, tended to progressively decrease with food deprivation. Results indicated that formal kinetic analysis can be applied to D-xylose absorption kinetics in horses. Reduction in the extent of D-xylose absorption after food deprivation may be partly caused by decreased rate of D-xylose absorption across the small intestinal mucosa, but other factors, such as gastric emptying and nonabsorptive losses, may also be involved.

Multicompartmental analysis was applied to study the kinetics of D-xylose distribution after IV administration to healthy mares deprived of food for 12 and 96 hours. Urinary excretion of D-xylose was measured over a 15-hour period after administration. The plasma D-xylose concentrations in this study were in the range found after oral tolerance testing. The disposition of D-xylose was described by a two-compartment model with linear kinetic characteristics. Total volume of distribution decreased significantly (P < 0.025) from 0.270 L/kg of body weight after the 12-hour period of food deprivation to 0.235 L/kg after the 96-hour period. Fractional rate of transfer between the central and peripheral compartments did not change after 96 hours without food. Approximately a third of the D-xylose administered was recovered in the urine. Difference in urinary elimination between the 12- and 96-hour periods was not significant. Nonrenal elimination rate was determined to be twice the renal elimination rate. The results indicated that formal kinetic analysis can provide useful information about D-xylose distribution in horses. The decreased D-xylose space found after a 96-hour period of food deprivation would tend to increase the plasma D-xylose concentration, and this may help in the interpretation of the D-xylose absorption test applied to anorectic horses.

Vancomycin hydrochloride was infused intravenously (i.v.) over a 30-min period in five horses at doses of 6.6, 11.0 and 15.4 mg/kg. Vancomycin concentration in plasma and synovial fluid samples was measured using a polarization immunoassay. A pharmacokinetic model was developed to accommodate the special features of the present study. The data were described by a two compartment open model with synovial fluid as an additional compartment in exchange with plasma. Minimum inhibitory concentration (MIC) and minimum bacterial concentration (MBC) were measured for Staphylococcus aureus and Enterococcus sp. using isolates from hospital patients. Based on the pharmacokinetic model and MIC/MBC data, a practical therapeutic protocol for vancomycin administration was established at doses of 4.3-7.5 mg/kg given as a 1-h infusion every 8 h.

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.

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.

Plasma antithrombin-III (AT-III) values were determined in 74 healthy horses by an automated spectrophotometric assay. The mean plasma AT-III value was 218% +/- 18% of normal human plasma. Plasma AT-III values did not differ significantly (P less than 0.05) among Thoroughbred, Standardbred, Quarter Horse, and other breeds or among mares, geldings, or stallions.